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This study was conducted to determine whether 100% FiO2 during hemorrhage would improve maintenance of mean arterial blood pressure and to assess the cardiovascular, arginine vasopressin, and renin-angiotensin system roles in the response. This also allowed evaluation of FiO2 effects on the baroreceptor control of these hormone systems. Six conscious female goats were hemorrhaged (0.5 mL x kg(-1) x min(-1)) for 30 minutes, while breathing 11%, 21%, or 100% O2. Mean arterial blood pressure was maintained only when the goats breathed 100% O2. FiO2 did not affect O2 consumption or delivery during hemorrhage. Increases in renin and arginine vasopressin were equal or reduced with 100% FiO2 and therefore did not contribute to the improved mean arterial blood pressure maintenance. Inspiration of 100% FiO2 during hemorrhage, therefore, may improve perfusion pressure with no changes in O2 consumption or delivery. Also, 100% FiO2 eliminated the negative correlation between both hormones and right atrial pressure, suggesting altered baroreceptor control of the hormones. [ABSTRACT FROM AUTHOR]

Purpose: Demands of medical residency training would be expected to result in physical deconditioning. This study determined the effects of residency on physical fitness.Methods: A prospective cohort study of the change in physical conditioning during residency using the Army Physical Fitness Test as a standardized measure of fitness was conducted. Ninety-four active duty U.S. Army physicians were followed during their medical residency training from July 1999 to June 2002. Army Physical Fitness Test results from interval tests performed throughout residency were compared to baseline results at matriculation. Changes in total score, number of push-ups and sit-ups completed in 2 minutes, 2-mile run time, and weight were recorded. Correlations between initial and final scores were evaluated.Results: All measured parameters worsened with statistical significance noted in the weight (p < 0.01), push-ups (p < 0.05), and 2-mile run (p < 0.01). Statistically significant negative correlations between initial and subsequent tests were noted in push-ups (p = 0.004), sit-ups (p = 0.0003), and total score (p = 0.0192).Conclusions: Physical fitness declines during medical residency training. This effect is most notable in residents with higher levels of fitness at the start of medical education. Further studies are necessary to evaluate for a similar decline among civilian residents. [ABSTRACT FROM AUTHOR]

Introduction: Hyperbaria-induced diuresis is accompanied by decreased basal and stimulated release of arginine vasopressin (AVP) and decreased blood volume possibly contributing to the reported orthostatic intolerance. Since hyperosmolality is not a consistent finding, the explanation of blood volume reduction at hyperbaria must involve an osmotic component to the diuresis. Investigations of a possible involvement of atrial natriuretic peptide (ANP) to the hyperbaric diuresis have revealed mixed results., Methods: Urinary excretion of electrolytes, AVP, and aidosterone were measured in four male subjects studied at 1 atmosphere absolute (ATA) and at 46 and 37 ATA (0.5 atmospheres pressure O2: 5% N2: remainder He) during a 35-d saturation dive. Also, the supine and 90 degrees tilt-stimulated plasma levels of AVP, plasma renin activity (PRA), and aldosterone, and the suppressed responses of ANP and the cardiovascular responses to tilt were determined at these pressures., Results: Tilt-stimulated levels of PRA were increased two- to threefold and the AVP response was eliminated throughout hyperbaria, except in two episodes of tilt-induced syncope where AVP was elevated 10- to 20-fold. This pattern supports most previous reports. Contrary to some reports, both supine and tilt-suppressed levels of ANP were reduced by about 50% at all three tilt experiments conducted at hyperbaria compared to predive control values., Discussion: These results suggest an altered ANP response at pressures of 37 ATA or greater, which is consistent with an appropriate ANP response to blood volume reduction and further suggest that the hyperbaric diuresis is not dependent on increased ANP.

AVP synthesis, storage, and osmotically stimulated release are reduced in young adult rats exposed prenatally to ethanol (PE). Whether the reduced release of AVP to the osmotic stimulus is due to impairment of the vasopressin system or specifically to an osmoreceptor-mediated release is not known. The present experiments were done, therefore, to determine whether a hemorrhage-induced AVP response would also be diminished in PE-exposed rats. Pregnant rats were fed either a control liquid diet [no prenatal ethanol (NPE)] or a liquid diet with 35% of the calories from ethanol from days 7-21 of pregnancy. Offspring were weaned at 3 wk of life. At 11 wk of age, femoral arterial catheters were surgically placed, and blood volumes were determined at 12 wk. Three days later, two hemorrhages of 10% of the blood volume were performed with samples taken before and 10 min after the hemorrhages. After a 20% blood loss, plasma AVP was 19% higher in NPE rats than in the PE rats despite no differences in mean arterial blood pressure (MABP). Also, hypothalamic AVP mRNA and pituitary AVP content were reduced in PE rats. Furthermore, confirming an earlier report of sex differences in AVP release, the hemorrhage-induced hormone response was twofold greater in female rats than male rats, regardless of previous ethanol exposure. These studies demonstrate that the AVP response to hemorrhage is reduced in PE rats independently of differences in MABP. The data are compatible with a theory of a reduced number of hemorrhage-responsive vasopressinergic neurons capable of stimulated AVP release in PE rats.

Reference values of blood volume (BV) and plasma volume (PV) of animal species are given as functions of body weight and gender specification generally is not given. Considering the common observation of a decreased hematocrit (Hct) in the females of many species, the BV, the PV, or both must differ between genders. The present study was performed to determine the magnitude of those differences. We measured Hct and PV in 24 female and 23 male Sprague-Dawley rats in their 12th week of life. The rats were surgically prepared with indwelling femoral arterial catheters 4 d prior to the determination of BV. Evan's Blue dye dilution was used to determine PV in conscious, quietly resting animals. BV was calculated as PV/(1-Hct). Mean Hct was 2% lower in female rats than males, and PV (mean +/- 1 standard deviation) was 4.86 +/- 0.54 ml/100 g in females compared with 4.12 +/- 0.32 ml/100 g in males. Calculated BV in female rats was 7.84 +/- 0.70 ml/100 g compared with 6.86 +/- 0.53 ml/100 g in males. When precise estimates of BV or PV are needed for research or dosing purposes, gender differences of 18% for PV and 14% for BV must be considered. In addition, species other than the rat may have similar discrepancies between sexes, and the prudent investigator must determine individual volume assessments of both sexes before assumptions of BV and PV for a species can be made.

Chronic consumption of ethanol in adult rats and humans leads to reduced AVP-producing neurons, and prenatal ethanol (PE) exposure has been reported to cause changes in the morphology of AVP-producing cells in the suprachiasmatic nucleus of young rats. The present studies further characterize the effects of PE exposure on AVP in the young adult rat, its hypothalamic synthesis, pituitary storage, and osmotically stimulated release. Pregnant rats were fed a liquid diet with 35% of the calories from ethanol or a control liquid diet for days 7-22 of pregnancy. Water consumption and urine excretion rate were measured in the offspring at 60-68 days of age. Subsequently, the offspring were infused with 5% NaCl at 0.05 ml.kg(-1).min(-1) with plasma samples taken before and at three 40-min intervals during infusion for measurement of AVP and osmolality. Urine output and water intake were approximately 20% greater in PE-exposed rats than in rats with no PE exposure, and female rats had a greater water intake than males. The relationship between plasma osmolality and AVP in PE-exposed rats was parallel to, but shifted to the right of, the control rats, indicating an increase in osmotic threshold for AVP release. Pituitary AVP was reduced by 13% and hypothalamic AVP mRNA content was reduced by 35% in PE-exposed rats. Our data suggest that PE exposure can cause a permanent condition of a mild partial central diabetes insipidus.

Objective: The goal of this study was to determine attitudes toward oral contraceptive pill (OCP)-induced amenorrhea among U.S. Army women., Methods: A volunteer sample (N = 154) of Army Active Duty, Reserve, and National Guard women completed an anonymous survey., Results: Desire for temporary amenorrhea was high with 86% (+/- 6%, 95% confidence interval [CI]) and 83% (+/-6%, 95% CI) desiring amenorrhea during field training and deployments, respectively. Fifty-four percent were unaware that OCPs can induce amenorrhea; only 7% (+/-4%, 95% CI) have used this practice during deployment. If made available with education, 49% (+/-8%, 95% CI) would use this practice. Logistic burdens of menstruation were associated with higher rates of desirability for OCP use with soldiers desiring OCPs rating their inconveniences significantly higher than those who did not desire OCPs (p < 0.05)., Conclusion: Although a significant number of soldiers desire OCP-induced amenorrhea, a large deficit in knowledge exists. Routine education as an Army-wide standard is warranted.

Estrogen and progesterone interference with renal actions of arginine vasopressin (AVP) has been shown. Thus we hypothesized that women will have a higher water turnover than men and that the greatest difference will be during the luteal phase of the menstrual cycle. Seven men (32 +/- 3 yr) and six women (33 +/- 2 yr) drank 12 ml water/kg lean body mass on different days at 0800 and at 2000 following 10 h of fast and a standardized meal at 0600 and 1800. Women participated on days 4-11 and 19-25 of the menstrual cycle. Initial urine and plasma osmolalities and urine flow rates were similar in all experiments. The cumulative urine voided over 3 h following the morning drink was less in men (73 +/- 12% of the water load) compared with women in either the follicular (100 +/- 3%) or luteal phases (102 +/- 10%) of the menstrual cycle. Nighttime values (30-43% of the water load) were lower in all experiments and were not different between sexes or menstrual cycle phases. Plasma AVP was higher at night and may contribute to this diurnal response. The data are generally consistent with the stated hypothesis; however, possibly owing to the greatly reduced urine flow in both sexes at night, a difference between sexes was not observed at that time.

Background: The hydrostatic pressure gradient during head-out water immersion (HOI) causes a blood shift from the legs into the thoracic cavity to stretch the receptors in the cardiac atria and results in a diuresis in hydrated subjects. The present study was conducted to examine whether the HOI-induced diuresis and related circulatory and hormonal changes were attenuated in the subjects who had no legs (legless men)., Methods: Two legless men served as the subjects. They lost both legs 15 and 17 yr ago by accidents and were otherwise healthy. Six normal males participated as controls. The experimental protocol was consisted of a 1-h control, a 3-h HOI (water temperature, 34.5 degrees C) and a 1-h recovery., Results: Average urine flow (0.6 ml x min(-1)), urinary excretion of sodium (90 microeq x min(-1)), and osmolal clearance (1.4 ml x min(-1)) of the legless subjects increased in the first h of immersion to 0.7 ml x min(-1), 139 microeq x min(-1), and 1.8 ml x min(-1), respectively. These values remained elevated during HOI, however, the magnitude of the increase was smaller compared with the control subjects. Plasma arginine vasopressin was significantly (p < 0.05) decreased from 1.0+/-0.4 microU x 100 ml(-1) to 0.4+/-0.2 microU x 100 ml(-1) during HOI in the normal subjects, but was not in the legless subjects (from 0.5 at control period to 0.4 microU x 100 ml(-1) during HOI). A concurrent reduction of aldosterone and plasma renin activity was observed with an increase in atrial natriuretic peptide during HOI in both subject groups, however, the magnitude of the changes was smaller in the legless subjects compared with the control subjects. Similarly, the average increase in cardiac output during HOI in the legless subjects (by 17%) was less compared with the control subjects (by 31%)., Conclusion: The magnitude of renal, endocrine, and cardiovascular changes in response to HOI in the legless subjects were less than in control subjects, but the responses were qualitatively similar. Accordingly, we suggest that the cephalad blood expansion during immersion is not only due to translocation of blood from the legs but also the abdominal region.

Objective: To determine the efficacy of azithromycin in the treatment of patients with typical cat-scratch disease., Design: Prospective, randomized, double blind, placebo-controlled clinical trial., Setting: Large military medical center and its referring clinics., Patients: Active duty military members and their dependents with laboratory-confirmed, clinically typical cat-scratch disease., Intervention: Study participants assigned by randomization to treatment with oral azithromycin or placebo for 5 days., Outcome Measures: Lymph node volume was calculated using three dimensional ultrasonography at entry and at weekly intervals. The ultrasonographer was blinded to the treatment groups. Endpoint evaluations were predetermined as time in days to 80% resolution of the initial total lymph node volume., Results: Demographic and clinical data showed that the azithromycin and placebo treatment groups were comparable at entry although the placebo group tended to be older. Eighty percent decrease of initial lymph node volume was documented in 7 of 14 azithromycin-treated patients compared with 1 of 15 placebo-treated controls during the first 30 days of observation (P = 0.026). After 30 days there was no significant difference in rate or degree of resolution between the two groups., Conclusions: Treatment of patients with typical cat-scratch disease with oral azithromycin for five days affords significant clinical benefit as measured by total decrease in lymph node volume within the first month of treatment.

During mixed gas saturation diving (to 3-49.5 ATA) daily urine flow increases by about 500 ml/day, with no changes in fluid intake and glomerular filtration rate. The diuresis is accompanied by a significant decrease in urine osmolality and increase in excretion of such solutes as urea, K+, Na+, Ca2+ and inorganic phosphate (Pi). The fall in urine osmolality is mainly due to a reduction of free water reabsorption which is associated with a suppression of insensible water loss and the attendant inhibition of antidiuretic hormone (ADH) system. The increase in urea excretion may be associated with a reduction of urea reabsorption at the collecting duct as a consequence of ADH suppression. The rise in K+ excretion is due to a facilitated K+ secretion at the distal tubule as a result of increased aldosterone, urine flow and excretion of impermeable anions such as Pi. The activation of aldosterone system is partly attributed to a transient dehydration induced by early hyperbaric diuresis. The increase in Na+ excretion in the face of enhanced aldosterone secretion indicates that the Na+ transport in the proximal tubule is markedly inhibited (by unknown mechanism). The Pi excretion increases with no changes in plasma level of parathyroid hormone (PTH), thus it may be due to an inhibition of Na(+)-Pi cotransport in the proximal tubule. The increase in Ca2+ excretion may be secondary to the inhibition of Na+ transport at the proximal tubule. Precise information on the proximal tubular Na+ transport is important to understand the mechanisms of impaired solute transport under hyperbaric conditions.

Background: Exercise increases plasma arginine-vasopressin (PAVP), plasma atrial natriuretic peptide (PANP), plasma renin activity (PRA), and plasma aldosterone (PALDO) in an intensity-dependent manner. With acute exercise, urine osmolality (UOSM) is often decreased despite increased PAVP. The hyperbaric environment lowers PAVP and UOSM, and increases urine flow., Hypothesis: If work produced similar renal effects at hyperbaria, greater than normal dehydration could result from larger free water losses., Methods: To test this hypothesis, hormonal and renal responses were assessed during exercise at 80% of maximum heart rate at 46 atmospheres absolute (atm abs) in 3 males, and during maximum exercise at 37 atm abs in 4 males., Results: This maximum exercise was performed at the highest pressure thus far reported and revealed no loss in peak power output. Maximum O2 consumption and heart rate were only slightly reduced, 9.5% and 7% respectively, despite a 41% reduction in maximum minute ventilation. Basal levels and the changes resulting from maximum exercise in PRA and PALDO were unaffected by pressure, but basal and exercise-stimulated levels of PANP and PAVP were reduced compared with 1.5 atm abs control values. UOSM was not significantly affected during maximal exercise at sea level, but during maximum exercise at 37 atm abs and submaximum exercise at 46 atm abs UOSM increased over 300 mosm.kg-1 and 180 mosm.kg-1, respectively., Conclusion: Contrary to the hypothesis, UOSM was increased by about 200 mosm.kg-1 by both exercise protocols during hyperbaric exposure and free water was conserved.

This study tested the hypothesis that airway relaxation to furosemide is mediated via the Na-K-2Cl cotransporter. If this mechanism exists in airway smooth muscle like in vascular smooth muscle, changes in airway relaxation should be associated with changes in Na-K-2Cl cotransporter function, and both should be substrate dependent. Tracheal rings from newborn guinea pigs were bathed in standard (STD) or varying low Cl- concentration ([Cl-]) N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES). Isometric relaxation to 300 microM furosemide or 10(-8) to 10(-5) M salbutamol was measured. Airway segments were incubated with rubidium-86 (86Rb) in STD or varying low [Cl-] HEPES, with and without 300 microM furosemide or 25 microM salbutamol. Furosemide was unable to reduce 86Rb uptake at 10 mM [Cl-], although relaxation was still observed in 10 mM [Cl-]. Salbutamol did not affect 86Rb uptake. This study demonstrated that there is a furosemide-sensitive Na-K-2Cl cotransporter in newborn guinea pig trachea. However, the effect of furosemide on cotransporter function did not always directly correspond to differences in relaxation, suggesting that the Na-K-2Cl cotransporter may play a major, but not exclusive, role in furosemide-induced airway relaxation.

Plasma arginine vasopressin (AVP) concentration is reduced in human subjects during prolonged saturation dive exposures of 4 atmospheres absolute (atm abs) and greater. The objectives of the present study were to determine if AVP would be reduced in eight male subjects during a 1-h exposure of 3 atm abs air and, if so, to determine the mechanisms responsible for the AVP response. Assessments of transmural central venous pressure (central venous pressure-esophageal pressure) and cardiac volume measurements were made to evaluate the possible role of cardiopulmonary receptors on the AVP response. Also, plasma osmolality (P(osmol)), venous blood gases, and mean corpuscular volume (MCV) were determined to evaluate potential effects of osmoreceptor and other fluid shifts on AVP release. AVP decreased (P < 0.05) by 0.5 microU/ml at 3 atm abs, whereas the transmural central venous pressure and cardiac volume remained unchanged throughout the experimental periods. A significant reduction (P < 0.05) in P(osmol) (by approximately 3 mosmol/kgH2O) was detected at 3 atm abs. Therefore, we conclude that the reduction in P(osmol) may cause the reduction in AVP during exposure to 3 atm abs pressure. The reduction in P(osmol) without water intake requires the postulation of an internal source of water. We propose that the threefold increase (P < 0.01) in venous PO2 and concomitant decrease (P < 0.05) in venous MCV suggest that the red blood cell may contribute to hypotonicity at 3 atm abs.

The hyperbaric environment causes a sustained diuresis accompanied by normal water intake and a decrease in insensible water loss. The maintained water intake may be necessary for the maintenance of water balance because of a reduced ability of the kidney to retain water, or may be causal in the diuresis. This problem was studied in four male subjects. Each ingested 1 liter of water (15 degrees C) at 0800 and 2000 h on different days, at 1 atm abs during a predive control, at 31 atm abs, and at 1 atm abs during the postdive control period. Urine was collected 30 min before and 3 h after the drink. Plasma vasopressin (VP) showed a circadian rhythm only at 1 atm abs, higher during the daytime. Because of this, and slightly lower VP levels at hyperbaria, a decrease in VP in response to the water load was significantly detectable only at 1 atm abs during the daytime. At 60 min after all water loads, there were no differences in plasma VP or plasma or urinary osmolality. Variability in the length of time of similarly reduced urine osmolality and increased free water excretion accounted for the increased urine flow during day compared to night (P < 0.05) at 120 and 150 min after the water load. The ability to excrete a water load both day (free water clear-ance, P < 0.05 at 60 min post-drink) and night (free water clearance, P < 0.05 at 60, 90, and 120 min post-drink) at 31 atm abs was enhanced. It is concluded that maintained water intake at hyperbaria is necessary to maintain water balance because there is a reduced ability of the body through renal mechanisms to retain a water load.

The possibility that the decreased urinary flow during continuous positive-pressure breathing (CPPB) may be a consequence of a reflex mediated via the cardiopulmonary baroreceptors to increase neurohumoral secretion or to change the sympathetic outflow was assessed. Muscle sympathetic nerve activity (MSNA) on the right peroneal nerve, vasoactive hormones, and renal and cardiovascular responses were measured during CPPB (+12 mmHg) in 10 male subjects (22.0 +/- 0.6 yr, 66.8 +/- 1.5 kg body wt). The experiments consisted of a 1-h control, 1 h with CPPB (experimental) or without CPPB (a time control), and a 1-h recovery period. Two blood samples were taken during each period for measurements of arginine vasopressin (AVP), plasma aldosterone (PAldo), plasma renin activity (PRA), norepinephrine, and atrial natriuretic peptide (ANP), and urine was collected hourly for the measurement of urine volume and electrolytes and clearances. MSNA rapidly increased (P < 0.05) at the onset of CPPB, continued to increase during exposure, and rapidly returned to the normal level at recovery. The MSNA changes coincided with increased plasma NE and were concurrent with a reduced (P < 0.05) urine output associated with a reduction of both free water and osmolal clearances, Na+ and osmolal excretions, and creatinine clearance (glomerular filtration rate). AVP and PRA increased (P < 0.05), whereas PAldo and ANP were unchanged. The results are consistent with the concept that increased sympathetic outflow may play a role in the reduction of urinary output and Na+ excretion during unloading of the cardiopulmonary receptors.

A practical method for chronic catheterization of the third cerebroventricular space in goats was developed by using a stereotaxic device. In female goats of various ages and weights, a stereotaxically mounted drill was positioned at an angle of 11.5 degrees with the tip of the drill bit located at a skull reference point 2 to 3 mm rostral to the posterior border of Bregma (intersection of the coronal with the sagittal sutures). The hole that was drilled served as the guide for a tight-fitting cannula, which was 20-gauge stainless steel with a stylet. The cannula was advanced by hand to a depth of approximately 40 mm from the top of the skull, positioning the cannula tip in the anterior region of the third ventricle anterior to the massa intermedia. Copious flow of cerebrospinal fluid verified appropriate positioning. The cannula was anchored with dental acrylic and a subcutaneous port system attached via plastic tubing. Cannula placement was assessed after surgery by use of fluoroventriculography. Cannula patency was maintained for 23 months. Minimal complications were seen, maintenance was minimal, and animals were allowed complete freedom of movement with no requirement for jackets or wraps and were used in several consecutive studies. No anesthetic complications were noticed.

Over the past decade several new routes of neurohypophysial hormone metabolism have been identified. These include nonhepatic splanchnic clearance and renal clearance in addition to filtration that appears to be receptor mediated. The intraluminal degradation of VP in the proximal tubule, and distal tubular secretion, at least in one species, has been identified. The brain has been identified as a site for VP and OT metabolism, and the amniotic sac may be a major site for VP clearance in the guinea pig fetus. There have been generalized findings regarding VP and OT metabolism. First, VP metabolism in the whole body and in the amniotic sac appears to increase with increasing concentrations of hormone; this does not appear to be the case with OT. Also, evidence has been presented that suggests a potential for the formation of biologically active metabolites. There have been several associations of pathophysiological states with altered VP or OT metabolism, sometimes with plasma levels remaining unchanged. Lastly, caution is emphasized when measuring these hormones by RIA, and differences in specificities of antisera toward hormone metabolites must be considered.

We studied hypoxia and hypotensive hemorrhage in conscious female goats. After control, goats continued an experimental period in normoxia or hypoxia [fractional inspired oxygen concentration (FIO2) = 0.10] for 120 min. After 60 min in the experimental period, a hemorrhage (0.5 ml.kg-1.min-1 for 30 min) was initiated (normoxic hemorrhage, NH; hypoxic hemorrhage, HH). Heart rate (HR) increased 51 +/- 18 beats/min with NH after 30 min of hemorrhage. HR increased 40 +/- 10 beats/min after hypoxic gas introduction, with no further increase during HH. Mean arterial blood pressure (MABP) was reduced 23 +/- 7 mmHg 30 min after completion of blood loss with normoxia but was reduced 23 +/- 7 mmHg at 20 min of HH. Arginine vasopressin (AVP) was increased to 2.60 +/- 2.08 and 160.40 +/- 49.74 microU/ml after 10 and 20 min of HH, respectively, and was only increased after 30 min (87.33 +/- 67.18 microU/ml) of NH. Unexpectedly, plasma renin activity (PRA) increased in parallel in both groups and was doubled at 30 min of hemorrhage. Atrial natriuretic factor was reduced to 8.8 +/- 1.6 pg/ml by 10 min of NH and to 11.4 +/- 3.3 pg/ml at 30 min of HH. Thus hypoxia leads to an earlier development of hypotension and increase in AVP with blood loss but may attenuate the PRA response to blood pressure reduction.

Urinary vasopressin (VP), aldosterone (ALDO), osmotic substances, sodium excretion, and plasma volume were assessed in 4 healthy male divers during 2 predive control days, 2 compression days, 6 days at 46 atm abs, and 26 days of decompression with stops at 37 and 27 atm abs. At pressure the ambient gas was trimix (0.5 atm abs O2:5% N2:remainder He). All urine was collected throughout the dive. Samples were divided into daytime (0700-1900) and nighttime (1900-0700). Indocyanine green dye dilution was used to determine plasma volume at predive 1, 46, and 24 atm abs. In agreement with previous dives at 31 atm abs, there was a decrease in VP excretion during compression lasting until return to 1 atm abs (P less than 0.05). Also similar to the shallower dives at 31 atm abs, the normal diurnal pattern of VP excretion, daytime higher than nighttime (P less than 0.05), disappeared at pressure. Urine osmolality showed alterations compatible with responses to VP. In contrast to previous studies at 31 atm abs, but in agreement with a previous study at 49.5 atm abs, there was no sustained increase in urinary ALDO excretion and only a transient natriuresis during the compression phase, followed by a reduced sodium excretion. In confirmation of earlier conclusions from indirect evidence, direct measurements of plasma volume indicated a reduction of about 20% (P less than 0.05) at 46 atm abs which remained reduced after decompression to 24 atm abs.

Four subjects were compressed to a simulated depth of 450 msw (46 bar) for 37 days in the main research chamber of the German underwater simulator diving facility at the GKSS Research Center, Geesthacht. The ambient gas was trimix. Urine was collected at 0700, 1300, and 1900 h each day for analysis of Na+, K+, volume, osmolality, and creatinine. Urine, antidiuretic hormone (ADH), and aldosterone were analyzed separately. Daily fluid, Na+, and K+ intake were analyzed throughout the dive. The aim of the investigation was to confirm the existence of a diuresis and natriuresis which had been observed in earlier saturation dives to 31 atm abs using He-O2. A significant diuresis was observed during compression despite a decrease in fluid intake. After compression the diuresis decreased somewhat but remained significantly above precompression control levels during the entire hyperbaric exposure. No significant change in fluid intake was observed. Daily Na+ and K+ excretion increased significantly during compression, which was accompanied by a significant increase in nocturnal excretion of Na+ and K+. Daily intake of Na+ and K+ decreased throughout the dive. Daily urine ADH decreased immediately upon compression and was associated with a parallel decrease in urine osmolality. In contrast, urinary aldosterone excretion exhibited no change during the dive despite the increase in Na+ and K+ excretion and decrease in Na+ intake.

We investigated the effect of negative pressure breathing during the inspiratory phase only (intermittent NPB) in 9 healthy male subjects who were in a sitting position and had no food or fluid intake for 12 h before the study. Intermittent NPB was without effect on urine flow and urinary sodium excretion but caused a significant increase in creatinine clearance. Plasma renin activity was significantly reduced, whereas plasma antidiuretic hormone (ADH), atrial natriuretic factor (ANF), and aldosterone levels were unaffected. To determine whether the blunted urinary response to intermittent NPB was a postural phenomenon, the study was repeated in 6 of the subjects while supine. Under these conditions there was a significant increase in urine flow and plasma ANF levels, but no change in all other measured variables. These results are consistent with a role for ANF, but not ADH, in the diuresis seen in supine subjects during NPB.

In the present study we compared the effects of Des Leu Angiotensin I (Des Leu AI) with Angiotensin II (AII) on the secretion of vasopressin (AVP) from the isolated hypothalamoneurohypophyseal system (HNS) and isolated posterior pituitary gland of the rat. Administration of 10(-6)M, 10(-5) M and 10(-4) M Des Leu AI was without significant effect on AVP secretion from the HNS. A similar phenomenon was seen in the posterior pituitary with 10(-6) M and 10(-5) M Des Leu AI, although 10(-4) M significantly increased AVP release. Administration of 10(-6) M AII was without significant effect in either preparation, although 10(-5) M and 10(-4) M AII caused significant dose-dependent increases in AVP secretion over control release that were similar in both the HNS and posterior pituitary gland. These results suggest that Des Leu AI is not a physiologically relevant stimulus of AVP secretion when restricted to this area of the rat brain. They are also consistent with the presence of receptors sensitive to AII in the pituitary gland of the rat.

A large-molecular-weight form of atrial natriuretic factor (ANF) was found in rabbit plasma. When extraction of plasma utilizing octadecylsilane cartridges is employed, this big ANF is not retained by the cartridge. When this material is dissociated with acid, immunoreactive ANF (irANF) is released. Of the acids tested, formic and acetic acid (0.05 M) were indicated as the most effective in causing the dissociation. High-performance liquid chromatography analysis of dissociated ANF, confirmed by coelution with synthetic peptides, disclosed the presence of ANF-(99-126) and ANF-(103-126) in a ratio of approximately 2:1. Atriopeptin I was detected in most of the samples analyzed, but atriopeptin II was only detected in one analysis. Despite the wide spectrum of the antiserum used for detection of irANF in the eluent fractions, only immunoreactive peaks coeluting with the four standards were detected. We therefore conclude that big ANF is a bound form of atrial peptides found in normal circulation.

Isolated rat kidneys were perfused with Krebs-Henseleit-bovine serum albumin solution at a mean pressure of 99 +/- 2.6 mmHg. After control periods, arginine vasopressin (AVP) was added to the perfusate at a final calculated concentration of 25 pg/ml (2.5 x 10(-11) M). Urine and perfusate samples were collected at 15-min intervals for the following 60 min to measure kidney function and the renal clearance of immunoreactive AVP (irAVP). At 15-30 min after the addition of AVP, total renal clearance of irAVP was 1,623 +/- 190 microliters.min-1.g kidney wt-1. Glomerular filtration accounted for 35 +/- 3.0% of the total clearance, and 65 +/- 10.3% was cleared by peritubular pathways. Of the filtered irAVP, 48 +/- 4.8% was recovered in the urine. To investigate the importance of V2 receptors in the metabolism of AVP, clearance measurements were made in the presence of the V2 antagonist [d(CH2)5,D-Ile2,Ile4,Arg8]AVP (5 x 10(-9) M). Total renal clearance of irAVP was reduced by 48% to 848 +/- 79 microliters.min-1.g-1. This reduction was entirely accounted for by the complete inhibition of peritubular clearance of irAVP. In the presence of the V2 antagonist, irAVP was cleared only by filtration. The proportion of filtered AVP recovered in the urine (53 +/- 8.7%) was not significantly altered by the presence of the V2 antagonist. We conclude that a major component of the renal clearance of AVP depends on receptor-mediated uptake of AVP in the kidney cells.

A stretch stimulus of the cardiopulmonary receptors results in a diuresis and natriuresis in dogs due to a suppression of renal sympathetic nerve activity. In the present experiment, the stretch stimulus in humans was given by means of continuous negative-pressure breathing (CNPB), and muscle sympathetic nerve activity (MSNA), renal responses, and hormones were measured to examine whether MSNA response during CNPB correlated with the usual renal and hormonal responses for stretch stimulus of the cardiopulmonary receptors. Nine healthy males were subjected to CNPB at -11 mmHg for 60 min. MSNA in the peroneal muscle nerve fascicles was measured continuously before (pre-CNPB), during, and after CNPB (post-CNPB). A step and sustained decrease (P less than 0.05) in MSNA (30 +/- 6% for burst frequency and 37 +/- 4% for total activity from pre-CNPB level) was observed during CNPB and it returned to pre-CNPB level at post-CNPB. Urinary excretion increased by 58 +/- 18% (P less than 0.05) during CNPB, and the diuresis was entirely osmolal in nature because of a significant increase (P less than 0.05) in Na excretion and a constant free-water clearance. The plasma level of norepinephrine decreased significantly (P less than 0.05) during CNPB and remained decreased (P less than 0.05) at post-CNPB. A twofold increase (P less than 0.05) in plasma atrial natriuretic peptide and a 35 +/- 9% reduction (P less than 0.05) in plasma renin activity were observed during CNPB, whereas no change was observed in plasma aldosterone and arginine vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal responses to low doses of atrial natriuretic peptide (ANP) may be potentiated during water immersion-induced central hypervolemia. To test this hypothesis, ANP was infused in awake dogs in doses of 0, 5, and 25 ng.kg-1.min-1 either when the dogs were in air or during head-out water immersion (WI) under thermoneutral conditions (37 degrees C). In general, there were greater diuretic (V) and natriuretic responses (UNaV) at the same level of plasma ANP in WI, with the slopes (or sensitivities) of V and UNaV in relation to plasma ANP levels being significantly increased during WI. Plasma renin activity decreased only during WI and was significantly correlated with both V and UNaV only during WI. Plasma and urinary arginine vasopressin levels were unchanged during WI. Infusion of ANP prevented the usual decline of hematocrit that occurs during WI. These results support the view that the renal sensitivity to ANP is augmented during the plasma volume expansion of WI. In addition, ANP may attenuate the transcapillary fluid shift that occurs during WI.

Intense training for long-distance running has been associated with reduced hemoglobin (Hb) levels and low iron stores. Whether iron supplementation helps prevent this "runner's anemia" remains controversial. To determine the relationship between iron status and the early stage of reduced Hb levels in male runners, we examined hematologic variables in 15 healthy men (ages 25 to 47 yrs) who ran twice their regular training distance in 20 days during a 500-km road race. Nine of the runners took iron-containing tablets which provided an average of 36 mg/d of iron, while the other six did not take iron supplements. Only one of the 15 subjects had a low Hb concentration (less than 14 g/dl) before the race. After 10 days (285 km), low Hb levels (p less than 0.001) were found in 12/15; six of these runners took iron supplements. However, following a 2-day rest period and five more days of running, only 5/15 and 7/15, respectively, had low Hb levels. Serum iron, ferritin, total iron binding capacity, and percent transferrin saturation values remained within normal limits and did not change significantly. Reticulocyte counts progressively increased, becoming 8-fold higher than at baseline (p less than 0.001), irrespective of the use of iron supplements. "Runner's anemia" developed in 11/15 (73%) of the subjects, independently of their iron status and iron intake. The reductions in Hb were accompanied by parallel decreases in RBC count and hematocrit, and by a significant reticulocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)

We examined the ontogeny of relaxation responses to three categories of calcium channel antagonists, represented by verapamil, diltiazem, and nifedipine, for both potential-operated (KCl-mediated) and receptor-operated channels [norepinephrine (NE)-mediated] in rat thoracic aorta. Aortic rings from 2- to 3-d, 1-wk, and 12-wk-old Sprague Dawley rats were mounted in an organ bath, bathed in Krebs' solution, and connected to a force-displacement transducer to measure isometric tension. Endothelium intact vessels at optimal passive force were exposed to a single ED50 of isotonic KCl or NE, equilibrium contraction was measured, then vessels were washed and exposed for 30 min to 1 microM verapamil, 1 microM diltiazem, or 0.1 microM nifedipine, followed by another dose of KCl or NE. Verapamil and diltiazem demonstrated significant (p less than 0.05) age-related increases in effectiveness for blocking KCl-mediated contraction [(% reduction of control contraction +/- SEM) (Verapamil: 2-3 d, 67.7 +/- 4.2; 1 wk, 72.5 +/- 1.8; 12 wk, 89.5 +/- 1.0. Diltiazem: 2-3 d, 64.6 +/- 2.9; 1 wk, 73.5 +/- 3.0; 12 wk, 83.1 +/- 1.8]. Nifedipine was equally effective at all ages: 2-3 d, 85.6 +/- 1.3; 1 wk, 90.0 +/- 1.6; and 12 wk, 91.3 +/- 1.4. Verapamil and diltiazem also showed significant age-related increases in effectiveness for blocking NE-mediated contraction (Verapamil: 2-3 d, 6.2 +/- 3.9; 1 wk, 28.0 +/- 4.8; 12 wk, 44.1 +/- 6.0. Diltiazem: 2-3 d, 8.0 +/- 3.1; 1 wk, 20.5 +/- 3.9; 12 wk, 46.5 +/- 4.8).(ABSTRACT TRUNCATED AT 250 WORDS)

Previous work indicates that the magnitude and direction of renal responses to exercise depend on the exercise intensity. To examine mechanisms responsible for these findings, renal and hormonal responses were studied in eight healthy male subjects (29.6 +/- 1.9 yr) before and immediately after four 20-min bouts of submaximal exercise (cycle ergometry) at work loads representing 25, 40, 60, and 80% of maximal oxygen consumption. Urine flow, osmotic clearance, glomerular filtration rate, and sodium excretion (UNa+V) all tended to rise at the 25% work load but were markedly reduced at the higher work intensities. Changes in urine flow paralleled changes in glomerular filtration rate (r = 0.91). Plasma vasopressin (ADH), aldosterone, and plasma renin activity tended to increase progressively with increases in work load, with the increases for all hormones reaching statistical significance when the level of exercise reached greater than or equal to 60% of maximal oxygen consumption. However, atrial natriuretic peptide was elevated (P less than 0.05) at all work loads from greater than 1.6-fold of control levels at the 25% work load to greater than 7-fold at the 80% work load. The increase in urine flow (6 of 8 subjects) and UNa+V (7 of 8 subjects) may be due to the increase in atrial natriuretic peptide and/or a 10% suppression (P less than 0.05) of ADH at the 25% work load.(ABSTRACT TRUNCATED AT 250 WORDS)

Hormonal, electrolyte, and renal responses were measured before, during, and after a marathon (42.2 km) in 14 runners: 8 young (Y) (mean age 27.8 yr) and 6 middle aged (MA) (mean aged 46.7 yr). No differences between groups in prerun values for heart rate (HR), plasma osmolality (OSM), antidiuretic hormone (ADH), aldosterone (ALDO), atrial natriuretic factor (ANF), or plasma renin activity (PRA) were found. Renal and urinary measurements were also similar between groups before the marathon. After 10 km of running, both groups had significant increases in HR, ALDO, ANF, and PRA, while OSM, Na+, and ADH remained unchanged from prerun values. The increase in plasma ANF concentrations at this point was significantly greater in the MA subjects compared with the Y (mean increase 104.1 vs. 42.8 pg/ml, respectively; P less than 0.01). Immediate postmarathon values for OSM, ADH, and Na+ were significantly higher than initial values in both groups, while HR, PRA, and ALDO continued to increase above the elevated levels found at 10 km. ANF values immediately postmarathon remained higher than prerun concentrations but were significantly reduced from those obtained at 10 km. In contrast, HR continued to rise until the completion of the run. These data are consistent with recent reports of an exaggerated ANF response in older subjects in response to central blood volume expansion.

Renal responses to head-out water immersion (WI) (37 degrees C, WI 100 min) were studied in conscious, instrumented dogs during volume repletion (R), when all blood and urine losses were replaced with 0.9% NaCl, or without volume repletion (NR), to determine the influence of hydration state. The lithium clearance method was used to estimate the locus of the renal tubular fractional sodium excretion (FENa) responses. WI in the R condition increased urine flow (V) from 0.9 (+/- 0.1 SE) to 4.2 (+/- 0.6) ml/min and FENa from 0.7 (+/- 0.1) to 3.2 (+/- 0.8)%. Fractional proximal sodium reabsorption (FPRNa) decreased from 0.82 (+/- 0.03) to 0.69 (+/- 0.1)% and fractional distal sodium reabsorption decreased from 0.96 (+/- 0.01) to 0.88 (+/- 0.04)%. By comparison, WI in the NR condition elicited smaller increments in V and FENa, no change in FPRNa and a significant decrease of FDRNa from 0.97 (+/- 0.01) to 0.93 (+/- 0.01). Although there were quantitative differences in the renal responses in the R and NR conditions, there were similar increments in both arterial and atrial pressures as well as plasma atrial natriuretic peptide concentration; plasma arginine vasopressin was unaltered in either situation, and plasma renin activity was depressed in both conditions. Since plasma protein concentration was significantly lower during the R condition, the differing renal responses are probably related to differing levels of volume expansion in the R vs. NR condition.

The present study was undertaken to determine the relative influence of the action of the central nervous system on the mechanism of water-immersion-induced diuresis by comparing physiological responses of quadriplegic (QP) and normal subjects. After overnight fasting seven male QP subjects with complete cervical cord transections (C5-C8) and six normal men were tested before, during, and after 3 h of head-out immersion (HOI) in thermoneutral water (34.5-35.0 degrees C). The reversible increase in urine flow and the total urine volume (309 +/- 53 ml in 3 h) in QP subjects were comparable with that of the normal subjects (318 +/- 96 ml in 3 h). While osmolal excretion was increased in QP subjects, its magnitude was less when compared with that of normal subjects. Instead, the increased urine flow in QP subjects was characterized by increased glomerular filtration rate (GFR) and free water clearance, in contrast to a predominantly osmotic diuresis with no changes in GFR in the normal subjects. The HOI elevated (P less than 0.05) systolic pressure only in QP subjects, whereas the increase in cardiac output was the same in both groups. While plasma renin activity and aldosterone responses to HOI in QP subjects were comparable with those of normal individuals, plasma atrial natriuretic factor (ANF) in QP subjects was twofold higher (P less than 0.05) during HOI, and the approximately threefold increase in ANF (P less than 0.05) in QP subjects due to HOI was the same as that of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Three male divers were studied for 2 days during each of the predive and postdive 1 ATA air control periods and for 7 days at 2.5 ATA (2.3 ATA N2 and 0.2 ATA O2). The chamber temperature was always maintained at a comfort level. Average urine flow remained at 1500 ml.day-1 during both predive and 2.5 ATA periods; urine osmolality also remained constant at around 700 mOSM/kg. On the other hand, daily excretion of Na increased significantly from 139 mEq during the predive period to 178 mEq at 2.5 ATA (P less than 0.05) but returned to the predive level during the postdive period. In contrast, daily K excretion decreased progressively with a significant decrease during the postdive period (P less than 0.05). Plasma osmolality, Na, and K remained unchanged, whereas a 6% reduction of total protein concentration at 2.5 ATA (P less than 0.05) was observed. A quantitatively similar decrease (8%) was observed for hematocrit during the 2.5 ATA period, which did not recover at postdive. These changes were accompanied by a significant increase in urinary excretion of antidiuretic hormone (P less than 0.05) and by decreases in both plasma renin and aldosterone (P less than 0.05) level and urinary excretion of aldosterone (P less than 0.05). Plasma atrial natriuretic factor remained unchanged throughout the entire dive period.

Three male divers were subjected to a 7-day dry saturation dive at 31 ATA (New Seatopia). Urine samples were collected for measurements of electrolytes and creatinine for glomerular filtration rate (GFR) 5 times daily, at 3-h intervals during daytime (0700-2200 h) and once at night (2200-0700 h). Collections were taken for 2 days before (predive 1 ATA air), 7 days during 31 ATA exposure, and during 10 days of decompression and for 2 days at postdive 1 ATA air. Blood samples were taken after overnight fasting at each of the dive periods for measurements of atrial natriuretic factor (ANF), electrolytes, and other blood constituents. Compression to 31 ATA resulted in a twofold increase in urine flow accompanied by increases in excretion of osmotic substances (+40%) and sodium (+54%), and a reduction in urine osmolality (-32%). The increase in urine volume was greater (P less than 0.05) at night than day with no change in GFR between day and night, confirming the earlier findings. However, no change in plasma ANF was observed in spite of a sustained increase in daily sodium and water excretion at high pressure. These results suggest that the hyperbaric diuresis-natriuresis may not be directly mediated by the ANF release.

This in vitro study examined the ontogeny of arginine vasopressin (AVP) and arginine vasotocin (AVT) compared with norepinephrine (NE)-mediated contraction in rat thoracic aortas. Aortas from three age groups (2-3 days, 6-7 days, and 12 wk) of Sprague-Dawley rats were used. Ring segment resting length was adjusted to optimize tension developed to a dose that produces half-maximal tension of NE in Krebs solution (pH 7.4, 37 degrees C) and gassed with 95% O2-5% CO2. Cumulative dose-response curves were generated for KCl (5-100 mM), NE (10(-10)-10(-5) M), AVP, and AVT (both 10(-10)-10(-6) M) in the presence and absence of a selective V1 vasopressinergic inhibitor, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin ([d(CH2)5Tyr(Me)]AVP). A progressive increase in sensitivity among all age groups was found for KCl and NE. There was a slight decrease in sensitivity to both AVP and AVT in the 1st wk. Maximum contractile response to NE increased between 2-3 and 6-7 days, whereas no change was observed for KCl, AVP, or AVT. AVP- and AVT-mediated contractions were selectively inhibited by [d(CH2)5Tyr(Me)]-AVP. These results suggest 1) receptor-mediated contractility is present from 2 days of age for NE, AVP, and AVT; 2) sensitivity to KCl and NE increases progressively during postnatal development, whereas sensitivity to AVP and AVT slightly decreases in the 1st wk with no progressive age-related increase by 12 wk; 3) AVP and AVT mediate contraction via a similar V1-like receptor.

HOI induces a significant increase in the cardiac output, which is accompanied by increases in the urinary excretion of water, Na and K. However, the renal responses are not always associated with the cardiac response, suggesting a possible dissociation of two events. Although the urinary excretion of both ADH and aldosterone decreases during HOI, the mechanism for these changes is not clearly understood. The renal responses to HOI, especially the natriuresis, is considerably attenuated in endurance-trained athletes, which may be related to the more moderate inhibition of both ADH and renin-aldosterone systems. The exact role of the cardiac receptors in inducing the renal responses to HOI is still not defined, although the latter receptors are involved in inducing the natriuresis. Finally, important diurnal variations have been demonstrated for the renal responses to HOI, and elucidation of the mechanism for this interesting phenomenon may help understand the overall mechanisms for the development of cardiorenal-endocrine responses to HOI.

Plasma vasopressin concentration (PAVP), renal function, and effectors of vasopressin release were evaluated in male volunteers during running at heart rates of 0, 35, 70, and 100% of maximum after 10 h abstinence from water (normal hydration) and at 100% after ingestion of 300 ml water. Plasma renin activity (PRA) and PAVP were linearly correlated and correlated to work intensity over all observations. Changes in PAVP were not correlated with changes in plasma osmolality (POSMOL) and plasma volume (PV) over all observations. Furthermore, despite similar changes in POSMOL, PV, PRA, body weight, mean arterial pressure, and plasma lactate concentration, the increase in PAVP after maximal exercise was greater during normal hydration than the water-supplemented state. Decreased urine flow observed in association with exercise was characterized by increased free water and decreased osmotic and creatinine clearances. Thus increased PAVP associated with exercise appears not to play a role in the concomitant antidiuresis. Vasopressin stimuli are probably variable at different times during exercise and may include factors other than those measured.

Comprehensive studies on body fluid balance on 5 divers were conducted during the Hana Kai II dive (17 days at 18.6 ATA and 7 days of decompression). Daily urine flow increased from about 2000 ml at 1 ATA to 2600 ml at 18.6 ATA, at 31 degrees C. This diuresis was accompanied by a reduction in urine osmolality (from 650 to 500 mOsm) and a slight increase in osmolal clearance. Endogenous creatinine clearance remained at about 173 ml/min throughout the dive. Despite such a sustained diuresis, neither daily water intake nor total body water volume changed significantly. The plasma renin activity changed little, while both plasma aldosterone concentration and urinary aldosterone excretion increased significantly during the first week at 18.6 ATA. The plasma prolactin concentration showed a significant decrease during the first 3 days at 18.6 ATA. The daily excretion of antidiuretic hormone (ADH) decreased significantly (by 40%) 4 days after compression and remained low throughout the rest of the dive. Insensible waterloss at 18.6 ATA was 35% lower than that at 1 ATA. It is suggested that the observed hyperbaric diuresis is due primarily to suppression of ADH as a result of suppression of insensible water loss.

Hypoxia alters the relationship of aldosterone secretion to plasma renin activity. The potential role plasma electrolytes play in this modification is not clear. This study analyzed the interrelationships among renin, aldosterone, vasopressin (ADH), and plasma electrolytes during 96 h of normobaric hypoxia. Eight ewes were exposed, in discrete experiments, to hypocapnic hypoxia [arterial O2 tension (PaO2) 37-42 mmHg, arterial CO2 tension (PaCO2) 26-28 mmHg] and eucapnic hypoxia (PaO2 40-43 mmHg, PaCO2 28-31 mmHg) by N2 dilution in an environmental chamber. Urine output (24 h) was measured, and arterial plasma samples were collected during the normoxic control period and at 24-h intervals of hypoxia. Plasma Na+, K+, renin, and ADH levels did not change from the normoxic values during either hypocapnic or eucapnic hypoxia. However, urinary aldosterone excretion [critical significance (alpha) less than 0.046] and K+ excretion (alpha less than 0.046) decreased markedly during each type of hypoxia. All sheep developed a pronounced negative K+ balance by 96 h of hypoxia. These data suggest that plasma K+ concentration is preserved by movement of K+ out of the intracellular compartment; this change in K+ distribution may inhibit aldosterone secretion during hypoxia.

Endurance exercise training alters the regulation of body fluids. To investigate specifics of these alterations, hormonal, electrolyte, and renal responses to water ingestion (1% of lean body wt) were studied in six moderately trained (T) and 6 untrained (UT) male subjects. No differences between groups for base-line hormonal, electrolyte, or renal measurements were found. After water ingestion, atrial natriuretic factor remained unaltered in both groups. Predrink plasma antidiuretic hormone (ADH) levels of 0.51 +/- (SE) 0.19 (UT) and 0.47 +/- 0.07 microU/ml (T) remained unchanged in the T group but were reduced from min 9 through 90 in the UT group. At 30 min postdrink, UT subjects had lower ADH values than T subjects (0.18 +/- 0.02 vs. 0.33 +/- 0.05 microU/ml), while plasma osmolality was similarly reduced by approximately 3 mosmol/kg in both groups. Urine flow rates increased in both groups from similar values of 0.85 +/- 0.24 (UT) and 0.67 +/- 0.11 ml/min (T) to peak flows of 4.6 +/- 1.6 for UT and 2.7 +/- 1.1 ml/min (T) to peak T, P less than or equal to 0.05) at 60 min postdrink. Urine osmolality was reduced from similar values of 809.1 +/- 62.1 and 867.0 +/- 56.1 mosmol/kg to values of 248.8 +/- 87.6 and 469 +/- 146.1 mosmol/kg for UT and T, respectively (UT vs. T, P less than 0.05), at 60 min. Reduced ADH before reductions in plasma osmolality in the UT but not the T subjects suggests that T subjects have a reduced oropharyngeal inhibition of ADH.(ABSTRACT TRUNCATED AT 250 WORDS)

Nine fasting, healthy, adult male volunteers were given oral carbohydrate before exposures to normoxia (PIO2 = 149 torr) and mild hypoxia (PIO2 = 98 torr). Following recovery, they were given oral ethanol before similar exposure to normoxia and mild hypoxia. Repeated measures of arterial blood and expired gases were made. Ethanol diminished respiratory gas exchange (R), causing lower alveolar and arterial oxygen pressures during normoxia and mild hypoxia and a reduction in arterial oxygen saturation from 89.9 to 87.4% during mild hypoxia. It is suggested that carbohydrates are preferable to ethanol and fats as nutrients during limited oxygen transport situations, such as high-altitude, carbon monoxide exposure, or during heavy exertion, and for patients with cardiovascular or pulmonary disease.

Cardiorenal-endocrine responses to 3-h head-out immersion (HOI) (water temperature = 34.5 +/- 0.5 degrees C) were studied during day (0900-1400 h) and night (2300-0400 h) in six hydropenic male human subjects. Although HOI induced a reversible increase in urine flow in all subjects, the response was faster and greater in magnitude during the day compared with night (P less than 0.05). Na excretion and osmolal clearance (Cosm) also followed the identical response pattern as urine flow, and in fact, the HOI-induced diuresis was entirely accounted for by the increased Cosm. Endogenous creatinine clearance was not different between the day and the night and remained unchanged during HOI. Both plasma renin activity and aldosterone concentration and urinary aldosterone excretion were nearly twofold greater during the day compared with night before HOI but decreased to the same level during HOI in both daytime and the nighttime series (P less than 0.05). There was no correlation between the Na excretion rate and renin-aldosterone levels either before or during HOI. Plasma antidiuretic hormone (ADH) level was comparable between day and night before HOI and decreased to a similar level during HOI in both daytime and nighttime series (P less than 0.05 for nighttime HOI). Cardiac output increased from 3.3 1/min before HOI to 5-6 1/min during HOI without showing any significant circadian difference. Hematocrit, hemoglobin, and plasma concentrations remained unchanged under all conditions. It is concluded that the renal response to HOI is subject to nocturnal inhibition, which cannot be attributed to circadian differences in the degree of HOI-induced central blood pooling, renin-aldosterone, or ADH responses.

Urinary excretion rate of antidiuretic hormone (UADHV) was studied in male volunteers in response to hypobaric hypoxia. The first series consisted of three groups. The chamber was decompressed to 465, 495, and 438 Torr during high-altitude (HA) exposure for groups I (n = 5), II (n = 5), and III (n = 4), respectively. In group I, the chamber air contained 3.77% CO2 to prevent alkalosis. The level of hypoxemia was similar in groups I and II. Mean 24-h UADHV was unchanged in group I, but increased 96% (P less than 0.05) and 180% (P less than 0.05) in groups II and III, respectively, on day 1 at HA and was normal during subsequent days at HA regardless of symptoms of acute mountain sickness. Shorter sampling intervals employed in a second series of experiments conducted at 495 Torr revealed a twofold increase in UADHV (P less than 0.05) 8-12 h after ascent in eight asymptomatic subjects; UADHV returned to base line within 9 h and remained low. The symptomatic subjects both had increased UADHV (3- and 8-fold from base line) between 2 and 4 h after ascent. Increased UADHV in asymptomatic subjects may be a result of the concomitant decrease in plasma volume, both of which appeared to be eliminated by CO2 supplementation.

The effect of the dopamine antagonist, haloperidol, on arginine-vasopressin (AVP) release induced by angiotensin II was studied in six dehydrated conscious dogs. Angiotensin II (10 ng/kg per min) alone caused a twofold increase (P less than 0.05) in plasma AVP concentration, a 25 mmHg increase (P less than 0.01) in mean arterial blood pressure (ABP) and a 70% decrease (P less than 0.01) in plasma renin activity (PRA). In the presence of haloperidol (3 micrograms/kg per min), angiotensin II caused similar changes in mean ABP (25 mmHg; P less than 0.01) and PRA (-65%, P less than 0.01), but a small insignificant decrease in plasma AVP (-22%). The AVP response to angiotensin II in the presence of haloperidol was significantly (P less than 0.05) different from its response to angiotensin II alone. Neither haloperidol alone nor the two vehicles had any effect on plasma AVP or mean ABP but PRA dropped slightly. The results suggest that a dopaminergic mechanism may be involved in angiotensin II-induced AVP release.

Renal and endocrine responses were studied in 10 male runners during a 20-day 500-km race. Overnight urine and prerun blood samples were taken prior to running on days 1, 2, 5, 8, 14, 17, and 20. Day 13 followed 70 h of rest. Urine flow rate, osmotic clearance, tubular free water reabsorption, urinary vasopressin excretion rate, and body weight were not significantly changed. Creatinine clearance was constant except for an elevation on day 5. Plasma osmolality was elevated on days 2, 14, and 17. Plasma sodium was increased (P less than 0.05) on days 2 and 13 but reduced on day 20. The percentage of filtered sodium excreted was significantly reduced on all nights following running and elevated on recovery day 13. Urinary aldosterone excretion rate was significantly elevated 162, 117, and 97% on days 5, 8, and 20 and returned to control levels on day 13 after 70 h of rest. These data suggest that in response to repeated long-distance running normal fluid balance is regained within 12 h. However, it is necessary to conserve sodium for at least 24 h after exercise as evidenced by the decrease in the percent filtered sodium excreted and continued elevation of aldosterone excretion.

The purpose of this study was to determine the relationship between plasma arginine vasopressin (PAVP) levels and the urinary clearance rate, the nonurinary plasma clearance rate, and the urinary excretion rate of AVP. Female conscious dogs were given an intravenous infusion of p-aminohippuric acid and inulin, and, after a 90-min control period, the infusion was either continued or AVP was added to the infusate to produce doses of 0, 40, 100, and 200 microU.kg-1.min-1 for the last 90 min of the experiment. The resulting PAVP levels were 1.2, 8.2, 11.4, and 21.6 microU/ml, respectively. The urinary clearance rate of AVP nearly doubled between the infusion rates of 0 and 100 microU.kg-1.min-1. Likewise, the nonurinary plasma clearance rate of AVP also nearly doubled between the infusion rates of 40 and 100 microU.kg-1.min-1. However, at the rate of infusion of 200 microU.kg-1.min-1, both the urinary and nonurinary clearance rates were unchanged compared with the 100-microU.kg-1.min-1 rate. The largest incremental rise in PAVP was observed between the doses of 100 and 200 microU.kg-1.min-1, when the clearance rates were apparently plateaued. The urinary excretion rate of AVP was linearly correlated with PAVP (R = 0.91) under the conditions of this study. The results suggest that the measurement of the urinary excretion rate of AVP is a reliable method of assessing PAVP and that the clearance of AVP increases when PAVP is elevated.