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For a person undertaking regular exercise, any fluid deficit that is incurred during one exercise session can potentially compromise the next exercise session if adequate fluid replacement does not occur. Fluid replacement after exercise can, therefore, frequently be thought of as hydration before the next exercise bout. The importance of ensuring euhydration before exercise and the potential benefits of temporary hyperhydration with sodium salts or glycerol solutions are also important issues. Post-exercise restoration of fluid balance after sweat-induced dehydration avoids the detrimental effects of a body water deficit on physiological function and subsequent exercise performance. For effective restoration of fluid balance, the consumption of a volume of fluid in excess of the sweat loss and replacement of electrolyte, particularly sodium, losses are essential. Intravenous fluid replacement after exercise has been investigated to a lesser extent and its role for fluid replacement in the dehydrated but otherwise well athlete remains equivocal. [ABSTRACT FROM AUTHOR]

Obese Zucker rats (OZR) are hyperinsulenemic, hyperglycemic and dyslipidemic and develop salt dependent hypertension. Since salt sensitivity is considered to be due to impaired handling of renal sodium excretion, these studies were conducted in the obese and lean Zucker rats (LZR) anesthetized with Inactin to evaluate renal function under basal conditions and during acute isotonic fluid volume expansion (VE). Mean Arterial blood pressure (MBP), heart rate (HR), renal blood flow(RBF) and glomerular filtration rate (GFR) were not significantly different between the lean Zucker rats fed normal diet or that fed salt rich diet(8% NaCl). However, basal UV and UNaV were significantly greater in the LZR fed high salt. During VE essentially identical increases occurred in GFR, UV and UNaV in both the lean groups. In the OZR fed salt rich diet also, there were no significant changes in the heart rate, RBF and GFR. However, arterial blood pressure of the OZR fed salt rich diet was significantly greater than that of the OZR on the normal diet as well as that of both the lean groups. Also, as in the LZR, basal UV and UNaV were significantly greater in the salt fed obese rats. During volume expansion there were no impairments in the ability of the obese groups fed normal or salt rich diet to eliminate sodium and water during volume load. In fact, the net sodium and water excretions during and 60 min after VE in both the obese groups were significantly greater than that of corresponding lean groups. Furthermore, these values in the OZR fed salt rich diet were significantly greater than that of the obese rats on normal salt diet perhaps due to the contribution of ‘pressure natriuretic mechanisms’. These data demonstrate that although OZR are salt sensitive, the renal mechanisms that would collectively respond to acute isotonic VE were fully functional. An unexpected and a novel finding in these studies is that the salt rich diet, in addition to increasing arterial blood pressure also significantly lowered plasma of insulin levels and enhanced glucose and cholesterol levels in the obese Zucker rats. [ABSTRACT FROM AUTHOR]

To assess effects of dietary salt on brain AT[sub 1] receptor densities, 4-wk-old Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats were fed a regular (101 µmol Na/g) or high (1,370 µmol Na/g)-salt diet for 1, 2, or 4 wk. AT[sub 1] receptors were assessed by quantitative in vitro autoradiography. AT[sub 1] receptor densities did not differ significantly between strains on the regular salt diet. The high-salt diet for 1 or 2 wk increased AT[sub 1] receptor binding by 21-64% in the Dahl S rats in the subfornical organ, median preoptic nucleus, paraventricular nucleus, and suprachiasmatic nucleus. No changes were noted in the Dahl R rats. After 4 wk on a high-salt diet, increases in AT[sub 1] receptor binding persisted in Dahl S rats but were now also noted in the paraventricular nucleus, median preoptic nucleus, and suprachiasmatic nucleus of Dahl R rats. At 4 wk on the diet, intracerebroventricular captopril caused clear decreases in blood pressure only in the Dahl S on the highsalt diet but caused largely similar relative increases in brain AT[sub 1] receptor densities in Dahl S and R on the high-salt diet versus regular salt diet. These data demonstrate that high salt intake rapidly (within 1 wk) increases AT[sub 1] receptor densities in specific brain nuclei in Dahl S and later (by 4 wk) also in Dahl R rats. Because the brain renin-angiotensin system only contributes to salt-induced hypertension in Dahl S rats, further studies are needed to determine which of the salt-induced increases in brain AT[sub 1] receptor densities contribute to the hypertension and which to other aspects of body homeostasis. [ABSTRACT FROM AUTHOR]

Uroguanylin is a peptide hormone that regulates sodium excretion by the kidney when excess NaCl is consumed. A new study demonstrates that mice deficient in uroguanylin have blunted urinary sodium excretion responses to oral sodium loads in addition to elevated blood pressure (see related article beginning on page 1244). A physiological role for uroguanylin is discussed, linking the intestine and kidney in an endocrine axis for the maintenance of sodium balance. [ABSTRACT FROM AUTHOR]

Renal hemodynamic and tubular responses to salt in women using oral contraceptives. Background. The use of oral contraceptives is associated with an increased risk of developing hypertension but the mechanisms of this hypertensive effect are not completely defined. The purpose of the present study was to assess prospectively the systemic and renal hemodynamic and tubular responses to salt in women taking oral contraceptives. Methods. Twenty seven young healthy normotensive women taking oral contraceptives containing monophasic combination of 30 μg ethynilestradiol and 150 μg desogestrel for>6 months were enrolled. All women were assigned at random to receive a low (40 mmol/day) or a high (250 mmol/day) sodium diet for 1 week on two consecutive menstrual cycles during the active oral contraceptive phase. At the end of each diet period, 24-hour ambulatory blood pressure, renal hemodynamics, sodium handling, and hormonal profile were measured. Results. The blood pressure response to salt on oral contraceptives was characterized by a salt-resistant pattern with a normal circadian rhythm. Salt loading results in an increase in glomerular filtration rate (GFR) (P < 0.05 vs. low salt), with no change in the renal plasma flow, thus leading to an increase in the filtration fraction (P < 0.05). At the tubular level, women on oral contraceptives responded to a low salt intake with a marked increased in proximal sodium conservation (P < 0.01 vs. high salt) and with an almost complete reabsorption of sodium reaching the distal tubule. After sodium loading, both the proximal and the distal reabsorption of sodium decreased significantly (P < 0.01). Conclusion. The use of oral contraceptives is not associated with an increased blood pressure response to salt in young normotensive women. However, oral contraceptives affect the renal hemodynamic response to salt, a high salt intake leading to an increase in GFR and filtration fraction. This effect is possibly mediated by the estrogen-induced activation of the renin-angiotensin system. Oral contraceptives also appear to increase the tubular responsiveness to changes in sodium intake. Taken together, these data point out evidence that synthetic sex steroids have a significant impact on renal function in women. The renal effects of oral contraceptives should be taken into account when managing young women with renal diseases. [ABSTRACT FROM AUTHOR]

Variation in osmoregulation is reported during water stress for 40 F3 families of Setaria italica L. (Foxtail millet). The lines were derived from a cross between two genotypes known to differ in this character. A clear separation was observed into 23 low and 17 high osmoregulation F3 families with coefficient variation 19.6%. Osmoregulation was not associated with plant height, length or width of flag leaf, length of panicle exertion, length or width of inflorescence or dry matter, but was significantly associated with grain yield, grain number and harvest index. Mean yield and harvest index for the high osmoregulation group were 1.58 and 1.57 times greater, respectively, than yield and harvest index for the low osmoregulation. [ABSTRACT FROM AUTHOR]

The present study was designed to test the hypothesis that renal nerves chronically modulate arterial pressure (AP) under basal conditions and during changes in dietary salt intake. To test this hypothesis, continuous telemetric recording of AP in intact (sham) and renal denervated (RDNX) Sprague-Dawley rats was performed and the effect of increasing and decreasing dietary salt intake on AP was determined. In protocol 1, 24-h AP, sodium, and water balances were measured in RDNX (n = 11) and sham (n = 9) rats during 5 days of normal (0.4% NaC1) and 10 days of high (4.0% NaCl) salt intake, followed by a 3-day recovery period (0.4% NaCl). Protocol 2 was similar with the exception that salt intake was decreased to 0.04% NaC1 for 10 days after the 5-day period of normal salt (0.04% NaC1) intake (RDNX; n = 6, sham; n = 5). In protocol 1, AP was lower in RDNX (91 ± 1 mmHg) compared with sham (101 ± 2 mmHg) rats during the 5-day 0.4% NaC1 control period. During the 10 days of high salt intake, AP increased <5 mmHg in both groups so that the difference between sham and RDNX rats remained constant. In protocol 2, AP was also lower in RDNX (93 ± 2 mmHg) compared with sham (105 ± 4 mmHg) rats during the 5-day 0.4% NaCl control period, and AP did not change in response to 10 days of a low-salt diet in either group. Overall, there were no between-group differences in sodium or water balance in either protocol. We conclude that renal nerves support basal levels of AP, irrespective of dietary sodium intake in normal rats. [ABSTRACT FROM AUTHOR]

The effect of nitric oxide (NO) on ion transport in the porcine proximal colon was investigated in slide-stripped epithelia mounted in Ussing chambers. The serosal addition of the NO-donors sodium nitroprusside (SNP, 0.5 mM) or S-nitroso-N-acetylpenicillamine (SNAP, 0.5 mM) induced a steep increase of short-circuit current ( I sc). The stimulatory effect of SNP on Isc could not be blocked by piroxicam or tetrodotoxin. Potassium channel inhibitors (quinidine, tetraethylammonium or barium) added serosally reduced the SNP- or SNAP-induced increases of Isc. In chloride-free solutions, the SNP-induced increase of Isc was smaller than in chloride-containing solutions. Cl- and Na+ flux measurements demonstrated that SNP diminished Cl- and Na+ net absorption. Pre-treatment with barium was able to block the inhibitory effect of SNP on NaCl net absorption totally. NO effects on paracellular pathways were assessed by measuring flux rates of [14C]-D-mannitol. SNP did not change unidirectional D-mannitol flux rates. In conclusion, NO inhibits NaCl net absorption in the proximal colon of pigs by acting directly on the enterocyte. The antiabsorptive (and/or prosecretory) effect of NO depends on a functional basolateral potassium conductance. [ABSTRACT FROM AUTHOR]

Split lamellae of posterior gills of Chasmagnathus granulatus adapted to 2.5‰ salinity were mounted in a modified Ussing chamber. With NaCl-saline on both sides of the preparation a transepithelial voltage (V[sub te]) of 4.1±0.5 mV (outside positive) was measured. After voltageclamping, the negative short-circuit current (I[sub sc]) amounted to -142±211µAcm[sup -2] at a conductance (G[sub te]) of 44±5 mS cm[sup -2]. Substitution of either chloride (by nitrate) or sodium (by choline) on both sides of split gill lamellae significantly reduced I[sub sc] (by 70-80%) and G[sub te] (by 30-50%). External CsCI (but not BaCl[sub 2] or furosemide) inhibited the negative I[sub sc] without affecting G[sub te]. Addition of ouabain, BaCl[sub 2] or diphenylamine-2-carboxylate to the internal bath inhibited I[sub sc] at unchanged G[sub te]. Internal acetazolamide did not affect I[sub sc] or G[sub te] across split gill lamellae. Unidirectional Na[sup +] influx across isolated and perfused posterior gills, however, was reduced by internal acetazolamide by approximately 20% at constant V[sub te]. The results suggest that posterior gills of hyperosmoregulating C. granulatus display a high conductance epithelium that actively absorbs NaCl in a coupled way by an electrogenic mechanism similar to that seen in the thick ascending limb of Henle's loop and, to a minor degree, by an electroneutral mechanism, presumably via apical Na[sup +]/H[sup +]and Cl[sup -]/HCO[sub 3]-antiports. [ABSTRACT FROM AUTHOR]

Presents letters to the editor on medical topics as of January 25, 2003. Call for Prime Minister Tony Blair of Great Britain to prevent escalating violence and a war in Iraq; Use of computers and information technology by physicians; Perception that medical management needs to be re-thought in Britain; Risk factors for sudden infant death syndrome which increase danger from infection; The long-term effects of advice to reduce dietary salt; Objections of Indian scientists to the export of human tissue for research; Idea that an ethics dialogue between rich and poor countries is needed; Complication of issues relating to abortions in Nigeria.

The plasma 25-hydroxyvitamin D concentration of Dahl salt-sensitive rats (S) is markedly decreased in response to high sodium chloride (salt) intake. We tested the hypothesis that urinary excretion is a mechanism for the decrease. Female S rats excreted 0.26 +/- 0.04 nmol 25-hydroxyvitamin D/24 h at wk 2 of high salt (80 g/kg) intake, five times that of female salt-resistant (R) rats at wk 2 of high salt intake and nine times that of S rats at wk 2 of low salt (3 g/kg) intake. The 25-hydroxyvitamin D binding activity in 24-h urine of S rats was 79 +/- 11 pmol/h at wk 2 of high salt intake, two times that in urine of S rats at wk 2 of low salt intake and > 35 times that in urine of R rats at wk 2 of low or high salt intake. We conclude that markedly decreased plasma 25-hydroxyvitamin D concentrations of S rats during high salt intake result in part from excretion of protein-bound 25-hydroxyvitamin D. Low plasma 25-hydroxyvitamin D concentrations in humans may also result in part from salt sensitivity, which is prevalent in > 50% of the United States hypertensive population. [ABSTRACT FROM AUTHOR]

The role of K+ in osmoregulation of the halophilic bacterium Halomonas elongata was investigated. At lower salinities (0.51 M NaCl), K+ was the predominant cytoplasmic solute (1.25 µmol mg protein–1). At higher salinities (1.03 M NaCl) ectoine became the main cytoplasmic solute (1.57 µmol mg protein–1), while the K+ content remained unchanged. In response to osmotic upshock, cells of H. elongata simultaneously accumulated ectoine and K+ glutamate. The ectoine and K+ glutamate levels in osmotically stressed cells exceeded the level of cells adapted to high salinities. The increase in K+ glutamate was long lasting (>120 min) and not transient, as described for non-halophiles. Regulation of the synthesis of ectoine and glutamate was proven to occur mainly at the level of enzyme activity. Limitation of K+ inhibited the growth of salt-adapted H. elongata cells, especially at high salinities, and caused a decrease of the intracellular organic solute content, inhibition of respiration, and an abolition of the cell's ability to respond to osmotic stress. The saturation constant KS for K+ was estimated to be 105 µM at a salinity of 0.51 M NaCl, indicating that an uptake system of medium affinity is responsible for K+ accumulation in H. elongata. [ABSTRACT FROM AUTHOR]

To test the role of epithelial Na channels in the day-to-day regulation of renal Na excretion, rats were infused via osmotic minipumps with the Na channel blocker amiloride at rates that achieved drug concentrations of 2-5 µM in the lumen of the distal nephron. Daily Na excretion rates were unchanged, although amiloride-treated animals tended to excrete more Na in the afternoon and less in the late evening than controls. When the rats were given a low-Na diet, Na excretion rates were elevated in the amiloride-treated group within 4 h and remained higher than controls for at least 48 h. Adrenalectomized animals responded similarly to the low-Na diet. In contrast, rats infused with polythiazide at rates designed to inhibit NaCl transport in the distal tubule were able to conserve Na as well as did the controls. Injection of aldosterone (2 µg/100 g body wt) decreased Na excretion in control animals after a 1-h delay. This effect was largely abolished in amiloridetreated rats. On the basis of quantitative analysis of the results, we conclude that activation of amiloride-sensitive channels by mineralocorticoids accounts for 50-80% of the immediate natriuretic response of the kidney to a reduction in Na intake. Furthermore, the channels are necessary to achieve minimal rates of Na excretion during more chronic Na deprivation. [ABSTRACT FROM AUTHOR]

Presents a study that examined whether short-term exposure to a high salt (HS) diet impairs acetylcholine (ACh)-induced vasodilation upstream from nitric oxide synthase. Effect of a short-term HS diet on ACh-induced dilation of rat arteries; Possible changes in the ACh signaling cascade that may contribute to any impaired vascular reactivity observed with a HS diet; Role of O[sup-sub2] radicals in contributing to impaired dilation in response to ACh in animals on a HS diet.

Looks at the relationship between elevated blood pressure (BP) in children and 24-h urinary excretion of sodium (Na) and potassium (K), and between BP and dietary salt intake. Measurement of 24-h urinary Na and K concentrations, systolic and diastolic BP, body weight and height; Weak correlation between Na excretion and systolic BP.

: BackgroundImpairment of renal dopamine excretion on high-salt diet (HS) may account for increased blood pressure (BP) in hypertensive subjects. Whether such impairment of dopaminergic activity exists in the adrenal gland is unknown. The purpose of this study was to differentiate degrees of dopaminergic inhibition of aldosterone secretion in patients with aldosterone-producing adenoma (APA).: MethodsA total of 15 patients with unilateral APA were fed a low-salt diet (LS) for 1 week, followed by another week on HS. At the end of each diet period, 24-h ambulatory BP recording, daily urine catecholamine measurement, and a metoclopramide test were performed.: ResultsA high-salt diet increased both daytime and nighttime BP (P < .001), and urine dopamine excretion (P < .01). Intravenous injection of 10-mg metoclopramide increased plasma aldosterone concentrations (PAC) on both diets. The areas-under-the-curve for PAC between LS and HS were not different, but the area-under-the-curve for PAC increment was greater on HS (P < .05). Six patients with increment areas on HS greater than those on LS by 50% were termed “suppressible,” and the remainders as “nonsuppressible.” On HS, the so-called suppressible subjects had greater urine dopamine and less urine norepinephrine excretions (P < .05). The nonsuppressible subjects had greater percentage increase of nighttime BP by HS than the suppressible (for systolic BP, 13.1% v 4.5%, P < .01; for mean BP, 12.0% v 5.1%, P < .01, respectively), but no difference in daytime BP.: ConclusionsTwo subtypes of APA were defined according to their responses to metoclopramide during salt manipulation. On HS, the nonsuppressible subjects, with less dopaminergic inhibition of aldosterone secretion, had less urinary DA excretion and greater BP elevation. The renal and adrenal dopaminergic activities are regulated in a parallel fashion. [Copyright &y& Elsevier]

We compared body temperature (Tb) daily rhythms in two populations of common spiny mice, Acomys cahirinus, during summer and winter months in relation to increasing dietary salt content. Mice were collected from the North and South facing slopes (NFS and SFS) of the same valley, that are exhibiting mesic and xeric habitats, respectively. During the summer, whilst mice were offered a water source containing 0.9% NaCl, SFS individuals had Tb peak values at 24:00, whereas NFS individuals had peak values at 18:00. When the salinity of the water source was increased, from 0.9 to 2.5% and then 3.5%, the difference between maximal and minimal Tb of both populations increased. In addition, with increased salinity, the Tb daily peak of SFS mice shifted to 18:00. During the winter, the mean daily Tb values of both populations of mice were lower than during the summer. At 0.9% salinity, the NFS mice exhibited a daily Tb variation with a peak at the beginning of the night. However, we did not detect any significant variation in daily Tb in the SFS mice. At 2.5% salinity, the difference between the mean daily Tb of mice from the two slopes increased. In winter we were unable to increase the salinity to 3.5% as the animals began to lose weight rapidly. We suggest that common spiny mice that inhabit these two micro-habitats are forming two discrete populations that respond differently to the environmental pressures prevailing in each habitat, by evolving different physiological capacities. [Copyright &y& Elsevier]

Discusses genetically defined forms of salt sensitivity and salt resistance in human monogenic diseases and in animal models mimicking pseudohypoaldosteronism type 1 or Liddle's syndrome. Role of the epithelial sodium channel (ENaC) in the human body; Health effects of an abnormal decrease of ENaC activity; Strategy that may be used to understand the pathophysiology of human diseases; Analysis of the long-term effects of salt intake as a risk factor.

The long-established association between high salt consumption and hypertension has led to calls for a reduction in salt intake. There is particular concern for the health status of Northern Irish consumers, who already have among the highest rates of coronary heart disease and stroke in the United Kingdom. With these concerns in mind, it is essential to establish the sources and patterns of salt consumption from discretionary and processed food sources before a reduction can be achieved. This study investigated differences in salt consumption patterns among consumers of varying socio-economic status. Research consisted of a consumer questionnaire (n = 360) distributed within Northern Ireland. The results of the study revealed high discretionary salt usage and frequent consumption of processed foods among consumers of lower socio-economic status. General observations from the questionnaire would suggest a need for improved health education for consumers in this group. The objective of health promotion should be to encourage a reduction in table and cooking salt usage and, in particular, in the consumption of highly salted processed foods. Enhanced product labelling is also encouraged to increase consumer awareness of current salt levels in food and of the availability of low-salt foods. In addition, the results of this study advocate further development activity in the production of product formulations with low-salt status. [ABSTRACT FROM AUTHOR]

High dietary salt intake decreases the endothelium-dependent dilation of skeletal muscle arterioles by inhibiting local nitric oxide (NO) activity without changing vascular smooth muscle responsiveness to NO. Under these conditions, microvascular walls show evidence of oxidative stress, and scavengers of reactive oxygen species (ROS) abolish this oxidative stress and restore normal arteriolar responses to acetylcholine (ACh). We tested the hypothesis that the salt-dependent appearance of microvascular ROS, and accompanying reduction in endothelium-dependent dilation, is due to a decrease in antioxidant enzyme expression or activity. We studied spinotrapezius muscle microvessels in rats fed normal (NS) (0.45%) or high (HS) (7%) salt diets for 4–5 weeks. Western analysis of arteriolar and venular protein showed no difference between groups in the content of superoxide dismutase (Cu/Zn SOD), catalase, or glutathione peroxidase. The catalase inhibitor 3-amino-1,2,4-triazole (3AT) increased arteriolar and venular oxidant activity (assessed by tetranitroblue tetrazolium reduction) by the same amount in both groups, suggesting similar levels of catalase activity. 3AT did not affect arteriolar responses to ACh in either group. The Cu/Zn SOD inhibitor diethyldithiocarbamate increased arteriolar and venular oxidant activity to a lesser extent in HS rats, suggesting reduced Cu/Zn SOD activity in this group. Cu/Zn SOD inhibition decreased arteriolar responses to ACh only in NS rats. These findings suggest that endogenous Cu/Zn SOD preserves the endothelium-dependent control of arteriolar tone in NS rats, and that a reduction in Cu/Zn SOD activity contributes to the loss of arteriolar NO activity in HS rats.Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Plasma sodium (Na+) concentration, i.e. natraemia, results from body tonicity equilibrium. During exercise, a change in body tonicity can result from an imbalance between intake and loss of Na+, potassium (K+) and water (H2O) due to renal and/or extra-renal mechanisms. Whether exercise-induced changes in kidney function could be responsible for such an imbalance was studied by measuring glomerular filtration rate (creatinine clearance), proximal tubule activity (lithium clearance) and renal handling of Na+ and K+ at rest and during exercise. Since hyponatraemia during or after exercise has been reported, we also investigated whether a water load could be appropriately excreted during exercise. Ten young men pedalled on a cycle ergometer at 60% of maximal oxygen uptake for 45 min with (HE, hydrated exercise) or without (DHE, dehydrated exercise) a supply of water. In both conditions, creatinine, lithium, and electrolyte (Na+ + K+) clearances decreased and natraemia did not change. The DHE induced a loss of body mass (-1.29%), decreased diuresis and large extra-renal water loss [mean (SEM)] [880 (73) ml]. The HE led to no loss in body mass, increased diuresis and lower extrarenal water loss [680 (48) ml]. Electrolyte-free water excretion, negative for DHE, represented 60% of diuresis during HE. Thus the kidney, by increasing electrolyte reabsorption mainly in the proximal tubule, and appropriately excreting a water load, seems efficacious in regulating extracellular fluid volume and body tonicity and so not responsible for the imbalance between (Na+ + K+)/H2O intake and loss. Therefore, extra-renal changes could be the main causes of exercise-induced tonicity imbalances which could ultimately lead to dysnatraemia. [ABSTRACT FROM AUTHOR]

Comments on the effects of high salt intake on blood pressure. Origins and economic impact of high salt intake; Analysis of pertinent topics and relevant issues; Implications on cardiology.

A comprehensive anatomical study was undertaken to examine the rectal salt gland in the Port Jackson shark, Heterodontus portusjacksoni, a shark known to invade estuarine environments. The microstructure and vascular organisation of the rectal salt gland was investigated using histological observation and scanning electron microscopy of vascular corrosion casts. Cellular specialisation was observed in the lining of the central lumen of this gland. This may indicate that there is some modification of the principal product of the gland prior to its secretion. The rectal salt gland has a complex structure related to its function. Contrary to previous reports, the flow in secretory tubules is in the opposite direction to that of the capillaries and thus constitutes a counter-current arrangement. The similarity in the organisation of the counter-current and lobulate arrangement of salt-secreting glands through phylogenetically diverse organisms, such as sharks and birds, suggests that this arrangement is important in achieving efficient salt secretion.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Assesses the hypothesis that angiotensin (ANG) II-induced hypertension is enhanced during high salt intake through stimulation of endothelin (ET) type A receptors by endogenous ET-1. Increase in the mean arterial pressure with continuous intravenous infusion of ANG II; Comparison of the effect of ANG II in rats on high salt intake with rats on normal salt intake.

Objective: To determine the possible relationship between insulin resistance and salt sensitivity in essential hypertension. Design and methods: We studied 17 non-obese, essential hypertensive patients (24-h blood pressure: 149 ± 15/94 ± 5 mm Hg) with normal glucose tolerance. Salt sensitivity was diagnosed in the presence of a significant increase (P < 0.05, more than 4 mm Hg) in 24-h mean blood pressure (MBP) when patients switched from a low-salt intake (50 mmol/day of Na[SUP+]) to a high-salt intake (240 mmol/day of Na[SUP+]), each period lasting 7 days. The insulin sensitivity index was determined by the euglycaemic hyperinsulinaemic clamp. Results: Six patients were classified as salt sensitive (24-h MBP increase: 6.2 ± 1.1 mm Hg), and 11 as salt resistant (24-h MBP increase: -1.2 ± 3.8 mm Hg). No significant differences were observed between salt sensitive and salt resistant patients regarding baseline characteristics, fasting serum insulin, fasting serum glucose, glycosilated haemoglobin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, uric acid and microalbuminuria. Salt sensitive patients exhibited a reduced insulin sensitivity index compared with salt resistant patients (1.7 ± 1.1 vs 3.5 ± 1.2 mg/kg/min; P = 0.009). An inverse relationship (r -0.57; P = 0.016) between the insulin sensitivity index and 24-h MBP increase with high salt intake was found. Conclusion: Salt sensitive essential hypertensive patients are more insulin resistant than salt resistant patients when both salt sensitivity and insulin resistance are accurately measured. Indirect measures of both insulin and salt sensitivity and/or the presence of modifying factors, such as obesity or glucose intolerance, may account for differences in previous studies. [ABSTRACT FROM AUTHOR]

The salt hypothesis is that higher levels of salt in the diet lead to higher levels of blood pressure, increasing the risk of cardiovascular disease. Intersalt, a cross-sectional study of salt levels and blood pressures in 52 populations, is often cited to support the salt hypothesis, but the data are somewhat contradictory. Four of the populations (Kenya, Papua, and two Indian tribes in Brazil) do have low levels of salt and blood pressure. Across the other 48 populations, however, blood pressures go down as salt levels go up, contradicting the hypothesis. Experimental evidence suggests that the effect of a large reduction in salt intake on blood pressure is modest, and health consequences remain to be determined. Funding agencies and medical journals have taken a stronger position favoring the salt hypothesis than is warranted, raising questions about the interaction between the policy process and science. [ABSTRACT FROM AUTHOR]

Determines the cellular mechanism of inhibition of NaCl absorption and the effect of steroids on this inhibition. Reduction of Na+/H+ exchange but not Cl-/HCO3- in the brush-border membrane of villus cells during chronic ileitis; Inhibition of Cl-/HCO3- exchange secondary to a decrease in the affinity for Cl-.

The purpose of this study was to determine if manipulation of dietary sodium could influence the severity of exercise-induced asthma (EIA). Fifteen clinically diagnosed EIA subjects participated in a double-blind, crossover trial. Subjects entered the study on a normal salt diet (NSD), and then were placed either on a low salt diet (LSD) or high salt diet (HSD) for two weeks. Each diet was randomized with a 1-wk washout between diets before crossing over to the alternative diet. Subjects performed a treadmill test to 90% of age-predicted maximum heart rate, and this exercise intensity was sustained for 5 min. Pre- and post-exercise pulmonary function tests were performed following each treatment period. 24-hr urinary sodium excretions were different (p<0.05) for all three diet periods (NSD=3630 mg/day,LSD=958 mg/day, HSD=8133 mg/day). Contrasting pre- to post-exercise changes in pulmonary function measurements, all forced expiratory volumes and flows improved on the LSD; FVC (+0.95 L), FEV1 (+0.4 L) and FEF25-75% (+0.83 L/s). The HSD induced reductions in FVC (-0.22 L), FEV1 (-0.37 L) and FEF25-75% (-0.55 L/s). In conclusion, a HSD caused an increase in severity of EIA, whereas a LSD represents a potential beneficial therapy for EIA subjects. [ABSTRACT FROM AUTHOR]

The morning surge in blood pressure (BP) is related to the morning occurrence of lethal cardiovascular events. We tested the hypothesis that salt intake may be associated with the morning surge in BP in essential hypertension. Seventy-six patients were admitted and placed on a low salt diet (2 g/day) for 7 days followed by a high salt diet (20-23 g/day) for another 7 days. At the end of each salt diet, 24-h ambulatory BP and heart rate monitorings and head-up tilt (HUT) test were performed. Patients whose average mean BP (MBP) was increased by more than 10% by salt loading were assigned to the salt-sensitive (SS) group (n = 37); the remaining patients, whose MBP was increased by less than 10%, were assigned to the non-salt-sensitive (NSS) group (n = 39). The increase in ambulatory MBP during 6.30-8.00 am above the baseline (2.00-4.00 am) was significantly enhanced by salt loading in the NSS group (P < 0.05), but not in the SS group. The coefficient of variation of 24-h MBP and heart rate was increased by salt loading only in the NSS group. The significant elevation of plasma noradrenaline concentration after awakening, which was noted during the low salt diet period, was unchanged during the high salt diet period in the NSS group, but abolished in the SS group. Salt loading enhanced HUT-induced decrease in systolic BP without affecting the heart rate response only in the NSS group. We conclude that the morning surge in BP is enhanced by salt loading in the NSS type of essential hypertension, presumably by the excessive activation of the sympathetic nervous system. [ABSTRACT FROM AUTHOR]

The article describes an exercise that solidifies manipulative learning for nephron physiology education by students using paper models of transporters and electrolytes in the basolateral and luminal membranes of nephron cells. The exercise provides opportunity to apply and test their own knowledge related to changes in physiological processes like water intake, excess of salt and blood volume alterations. They can also learn pathology like inappropriate antidiuretic hormone secretion.

Salt and water retention, a cardinal feature of nephrotic syndrome, was suggested to be an important factor leading to reduced diurnal blood pressure (BP) variation in renoparenchymal disease. Twenty-four hour BP (SpaceLabs SL 90207), 24-h urine excretion of cat-echolamines, plasma renin activity and plasma aldos-terone concentration were therefore determined in 10 nephrotic patients with normal serum creatinine levels (group A, serum creatinine 1.0 ± 0.2 mg/dl), in 10 nephrotic patients with increased serum creatinine levels (group B, serum creatinine 2.4 ± 0.9 mg/dl) and in 20 controls matched in respect of age and BP. To study the direct influence of fluid volume overload, diurnal BP variation was determined before and after volume depletion by ultrafiltration in 10 patients with end-stage renal failure. Diurnal BP variation was characterised by the difference of mean BP during daytime (10 pm to 8 am) and night-time (8 am to 10 pm). In group A, the systolic and diastolic day-night difference was not changed when compared with the controls (NS). In contrast, in group B the day-night difference was significantly lower than in the controls (P < 0.01). Twenty-four hour urine catecholamine excretion and plasma aldosterone were comparable between the study groups. Plasma renin activity, however, was significantly increased in group A (P < 0.05). Nocturnal BP drop was not related to plasma renin activity in the nephrotic patients. The blunted diurnal blood pressure variation in end-stage renal failure was not influenced by ultrafiltration. The study demonstrates that the blunted diurnal BP variation in kidney disease is unaffected by marked changes in total exchangeable sodium and fluid volume, but is sensitive to changes in glomerular filtration rate. [ABSTRACT FROM AUTHOR]

In non-pregnant individuals, a strong positive association of sodium intake with blood pressure has been established, but the relationship between sodium intake and blood pressure in human pregnancy remains obscure up to date. The aim of this prospective observational cohort study was to assess the relationship between urinary sodium excretion (as a measure for intake) and blood pressure from the early second trimester onwards throughout pregnancy. The study group consisted of 667 low-risk women with singleton pregnancies, of whom 350 were nulliparous and 317 parous. Blood pressure was measured in a standardised fashion at predetermined intervals from the first antenatal visit prior to 16 weeks gestation until delivery. Urinary sodium excretion was measured in 24-h urine collections on at least four occasions between 16 and 38 weeks gestation. Main outcome measures were the coefficients of correlation between changes in urinary sodium output and changes in blood pressure during six different gestational epochs. No significant correlations were found between changes in urinary sodium output and changes in blood pressure. Correlation coefficients were alike for nulliparous and parous women and for different gestational intervals. Prior to 32 weeks gestation, no differences were observed in sodium excretion between women who remained normotensive and those who developed gestational hypertension. These results suggest that changes in sodium intake are not associated with blood pressure changes in low-risk pregnant women. Blood pressure increases as observed in the second half of normotensive and hypertensive pregnancies are unlikely to be caused by changes in renal sodium handling. [ABSTRACT FROM AUTHOR]

Mechanosensitive channels are ubiquitous amongst bacterial cells and have been proposed to have major roles in the adaptation to osmotic stress, in particular in the management of transitions from high to low osmolarity environments. Electrophysiological measurements have identified multiple channels in Escherichia coli cells. One gene, mscL, encoding a large conductance channel has previously been described, but null mutants were without well-defined phenotypes. Here, we report the characterization of a new gene family required for MscS function, YggB and KefA, which has enabled a rigorous test of the role of the channels. The channel determined by KefA does not appear to have a major role in managing the transition from high to low osmolarity. In contrast, analysis of mutants of E.coli lacking YggB and MscL shows that mechanosensitive channels are designed to open at a pressure change just below that which would cause cell disruption leading to death. [ABSTRACT FROM AUTHOR]

Studies the effects of an increase of daily intake of sodium chloride (NaCl) on the renal cortical blood flow and blood flow to the inner and outer medulla. Methods used in the study; Effects of increasing NaCl intake to normal rats; Effects of increased NaCl intake with fixed plasma angiotensin (ANG) II in normal rats; Discussion on the results of the study.

Studies the roles of serotonin receptors in the lateral parabrachial nucleus and brain angiotensin type 1 receptors in the intake of sodium chloride and water induced by angiotensin II. Histological analysis; Effects of methysergide injections; Controls for the specificity of injection sites.

To investigate whether salt sensitivity is associated with differences in left ventricular mass or geometry, salt sensitivity testing and Doppler echocardiography was performed in 30 essential hypertensive patients (7 women and 23 men) with mean age 43 ± 9 years. Salt sensitivity was defined as a 10% increase or more in 24-h blood pressure (24hBP) when going from low to high dietary sodium intake based on a single test. Eight patients were characterized as salt sensitive and 22 as salt resistant. At baseline, there was no difference in casual blood pressure (156/103 ± 17/9 vs 158/100 ± 18/11 mmHg) or 24hBP (152/90 ± 25/15 vs 159/89 ± 19/8 mmHg), in duration of hypertension (5 ± 4 vs 4 ± 3 years), daily sodium excretion (144 ± 68 vs 171 ± 68 mmol), left ventricular mass (LVM) (212 ± 45 vs 246 ± 52 g) or left ventricular relative wall thickness (RWT) between the salt sensitive and salt resistant groups of patients. In the total study population, increased RWT was found in 17 patients, and increased LVM in 10 patients. In only 10 patients were both these variables normal. Left ventricular geometric pattern did not differ between the salt sensitive and salt resistant groups. LVM and RWT were significantly correlated with 24hBP (r = 0.57 and 0.51, respectively; both p < 0.01). Significant correlation was also found between LVM and casual blood pressure, blood volume, body surface area, serum creatinine and albuminuria (r = 0.53, 0.60, 0.54, 0.54 and 0.43, respectively; all p < 0.01). In multiple regression analysis, 24hBP and blood volume were identified as independent predictors of LVM (R[sup 2] = 0.51, p < 0.001). Conclusions: increased RWT or LVM is common in both salt sensitive and salt resistant essential hypertensive patients. Salt sensitivity status based on a single test does not influence left ventricular hypertrophy or geometry. Twenty-four-hour blood pressure is related to increased RWT and LVM. [ABSTRACT FROM AUTHOR]

The influence of isosorbide-5-mononitrate (IS-5-MN) on the cardiovascular effects of high dietary salt intake (NaCl, 6.6% of dry weight of food) and that of a potassium, magnesium and l-lysine-enriched salt alternative (Pansalt 10.5%, producing a 6.6% content of NaCl) was studied in spontaneously hypertensive rats in an 8-week experiment. Common salt produced a marked rise in blood pressure and induced cardiac and renal hypertrophy, while the salt alternative, although containing the same amount of NaCl, neither increased blood pressure nor caused any significant cardiac hypertrophy. IS-5-MN treatment at a daily dose of approximately 60-70 mg/kg (mixed with food) attenuated the rise in blood pressure induced by common salt, but did not prevent the cardiac or renal hypertrophy. IS-5-MN did not offer any additional benefit to the use of the salt alternative diet alone in treatment of high blood pressure. Mesenteric arterial responses in vitro were examined at the end of the study. IS-5-MN treatment during the moderately low-salt (NaCl 0.7%) control diet tended to decrease the contractile response to noradrenaline and increase the relaxation to acetylcholine. Common salt, but not the salt alternative, induced a 50% increase in the 24-h urinary excretion of cyclic GMP. Both salt supplements induced an 8-9-fold increase in the excretion of calcium, and about a 2-fold increase in the excretion of phosphorus. Common salt also increased the excretion of magnesium by 50%. IS-5-MN treatment had no significant effect on the excretion of the mineral elements. Our findings show that increased intake of potassium and magnesium reduces the harmful effects of common salt. Pressure-independent mechanisms are involved in salt-induced left ventricular and renal hypertrophy, since they remained unaffected despite the prevention of the salt-induced rise in blood pressure by IS-5-MN treatment. [ABSTRACT FROM AUTHOR]

In studies of the effects of salt intake on blood pressure (SBP, MBP, DBP), influences on heart rate (HR) are usually neglected even though the longterm load on both left ventricle (LV) and systemic arteries (SA) is better related to the product of HR × SBP (or MBP) than to pressure alone. After all, altered salt intakes often induce considerable volume-related changes in HR, and the heart operates more economically at low HR and high stroke volume (SV). Thus, about 3/4 of LV metabolism is used for the build-up of systolic tension, while the cost for SV expulsion, or for SV increases, is far lower. Moreover, low HR prolongs the diastolic period, so important for LV coronary supply. Against this background we have used results from studies in both rats and man, in which both BP and HR were followed during marked changes in salt intake, to explore how this affected the HR × SBP (or HR × MBP) product. Briefly, in ordinarily salt-resistant organisms, whether normo- or hypertensive, salt intake increases, which in man ranged from 10-20 to 250-300 mM (in rats over 100-fold), if anything reduced the computed longterm load (HR × SBP, or MBP) on LV and SA, as consequences of an efficient reflex volume control. By contrast, in salt-sensitive man, HR reflex reductions to increased salt intake were almost absent despite substantial SBP elevations, suggesting the influence of a CNS suppression of bulbar reflex centres combined with CNS neurohormonal interference with renal salt volume excretion, as in SHR. [ABSTRACT FROM AUTHOR]

Assesses the effect of a low-protein diet on NaCl intake. Subjects, maintenance and diets; Calcium appetite; Procedures; Statistical analysis.

Determines changes in Na+ or Cl- concentrations that affect the ability of human neutrophils (PMN) to mediate host defense against opportunistic bacteria. Ionic requirements for PMN function; Correlation between Pseudomonas aeruginosa culture in cystic fibrosis airways and compromised PMN function; Phagocytosis.

Investigates the effects of denervation of the carotid sinus and aortic arch baroreceptors on sodium depletion-induced salt appetite in rats. Injections of furosemide; Salt appetites of sham and sinoaortic baroreceptor-denervated rats; Hormonal afferent mechanisms of salt appetite.

Investigates the mutual relationship between acute osmotic stimulation and arginine vasopressin (AVP) gene expression in rats. Effect of acute salt loading on the time course of the AVP messenger RNA level in the hypothalamus and whole brain tissue; Measurements for hematocrit, plasma osmolality and plasma AVP.

Investigates thirst and taste palatability responses to ten different sodium chloride solutions during rehydration. Plasma osmolality and plasma sodium concentration; Measurement for thirst rating, renal fractional reabsorption of water and plasma arginine vasopressin concentration; Osmotically induced thirst.

Explores the alteration in salt preference of Fischer 344 (F344) rats with an expanded range of NaCl concentrations. Specificity of the chorda tympani nerve in mediating F344 salt aversion; Comparison with Wistar rats; Studies of glossopharyngeal nerve transections.

Determines the role of protein kinase C in the regulation of the mode of sodium chloride entry into Necturus gallbladder epithelial cells. Effect of amiloride on rate of swelling of cells exposed to ouabain; Effect of phorbol 12-myristate 13-acetate on ouabain-induced swelling and sensitivity to inhibitors; Effect of kinase inhibitor H-7 on PMA-treated tissues.