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Background Men with heart failure are reported to be less adherent to low-sodium diets than women are. One potential reason may be that men consume more food and, consequently, more sodium than women do. Objectives The aims of this study were to compare dietary sodium intake, urine sodium excretion, and sodium density of diet consumed between men and women with heart failure and to determine whether sex moderated the relationship of kilocalories (kcals) consumed with dietary and urine sodium. Methods A total of 223 patients with heart failure (mean age, 62 ± 12 years; 70% men, 46% New York Heart Association class III-IV) completed detailed 4-day food diaries and provided 24-hour urine sodium samples. To account for sodium density of food, dietary sodium and urine sodium were referenced to sodium per 1000 kcal. Results On an absolute basis, men consumed 23% more kcals and 28% more sodium than women did; 24-hour sodium excretion was 16% higher in men than in women. There were no differences between men and women when dietary sodium and urinary sodium were referenced to 1000 kcal, indicating they consumed foods with similar sodium density. However, both moderation analyses showed that the dietary sodium intake of men and women with lower kcal intake was similar, whereas men with higher kcal intake consumed more sodium-dense foods than women did. Conclusion The results suggest that the men with higher sodium intake than women had 2 reasons for nonadherence. They consumed more food and foods with higher sodium density than women did.

Introduction: Hypertensive patients have impaired sodium excretion. However, the mechanisms are incompletely understood. There is interaction between kidney and adipose tissue. Whether and how adiponectin, one of adipokines, contributes to impaired sodium excretion in hypertension has not been previously investigated. Hypothesis: Adiponectin promotes natriuresis and diuresis and their impairment is involved in hypertension. Methods: We used Wistar-Kyoto (WKY) rats, spontaneously hypertensive rats (SHRs), GRK4g142A>V transgenic mice to test the natriuresis-effect of adiponectin through intrarenal arterial infusion. Renal proximal tubule (RPT) cells, adiponectin knock out (Adipo-/-) mice, mutant plasmid were used. Results: We demonstrate that sodium excretion was reduced in Adipo-/- mice. The intrarenal arterial infusion of adiponectin induced natriuresis and diuresis in WKY rats, which was impaired in SHRs. Adiponectin inhibited Na+-K+-ATPase activity in RPT cells from WKY rats but not from SHRs. Increased adiponectin receptor phosphorylation and subsequent uncoupling from Gai, rather than altered adiponectin receptor expression, were responsible for the loss of adiponectin-mediated inhibition of RPT Na+-K+-ATPase activity, impaired natriuresis and diuresis in SHRs. Mutation of the AdipoR1 phosphorylation site restored its linkage to Gai and the adiponectin-mediated inhibition of Na+-K+-ATPase activity in RPT cells from SHRs. Finally, we identified G protein-coupled receptor kinase 4 (GRK4) as the cause of adiponectin receptor hyper-phosphorylation. GRK4g142A>V transgenic mice replicated the abnormal adiponectin function in SHRs, whereas down-regulation of GRK4 by renal-ultrasound directed siRNA restored the adiponectin-mediated sodium excretion and reduced the blood pressure in SHRs. Conclusions: The stimulatory effect of adiponectin on sodium excretion is impaired in hypertension, which is attributable to increased renal GRK4 expression and subsequent adiponectin receptor hyper-phosphorylation. Targeting GRK4/adiponectin receptor/Gai may restore the impaired adiponectin-mediated sodium excretion in hypertension, thus representing a novel strategy against hypertension.

Among ~25% of patients with essential hypertension (EH), circulating endogenous ouabain (EO) and aldosterone (Aldo) are typically coelevated and their BP is especially salt-sensitive (SS). We probed for exaggerated natriuresis in a large cohort (712) of hypertensive patients that underwent an acute 2hr (T 120 ) load with saline (0.9%/2 L). Results: Using a quartiles analysis of sodium excretion, the 4th quartile subgroups showed higher SBP and DBP at T 120 , and at 2 hrs recovery (T 240 ). Fractional sodium excretion (FE Na) was significantly higher during loading and recovery in the 4 th quartile subgroup. Plasma Aldo was suppressed after saline in all subgroups as expected. SS patients showed an increased EO. In the 4 th quartiles EO was elevated at baseline and after saline (see figure), p Manova > 0.001 and the urinary Na/K ratio output was higher. Further, increases in plasma Na + were greater in the 4 th quartile group (1.91 ± 0.15 vs 0.83 ± 0.13 mM, p

Premenopausal women have a lower risk of hypertension compared to age-matched men. Recently, prominent roles have been assigned to P2Y 2 and P2Y 4 purinoceptor subtypes in promoting Na + excretion, implicating dysfunction of these receptors as potential contributors to hypertension. We recently reported that activation of P2Y 2 and P2Y 4 receptors in the renal medulla by UTP promotes Na + excretion in male rats. In intact females, UTP did not stimulate Na + excretion while ovariectomy unmasked UTP-induced natriuresis. These observations led us to hypothesize that intact females have higher basal renal medullary activity of P2Y 2 and P2Y 4 receptors in regulating Na + excretion compared to male and ovariectomized (OVX) rats. To test that, we determined (i) P2Y 2 and P2Y 4 mRNA and protein expression in the inner medulla from male, intact female and OVX Sprague Dawley rats and (ii) the effect of inhibiting medullary purinoceptors (P2 receptors) on Na + excretion in those rats. We found that P2Y 2 and P2Y 4 mRNA expression was higher in the inner medulla from females compared to males (1.00±0.09 vs. 0.70±0.05 and 1.00±0.22 vs. 0.29±0.05, respectively, P2 and P2Y 4 mRNA expression were eliminated by ovariectomy (0.60±0.06 and 0.29±0.04, respectively, p2 receptor, compared to males. In anesthetized rats, medullary P2 receptor inhibition by suramin (P2 receptor antagonist, 750 μg/kg/min) significantly attenuated Na + excretion in intact females (0.4±0.1 vs. 0.9±0.2 μmol/min, P2 ) increases the expression of P2Y 2 and P2Y 4 receptors, we subjected cultured mouse inner medullary collecting duct cells (mIMCD3) to different concentrations of E 2 (0, 10, 100 and 1000 nM). We found that E 2 dose-dependently increased the expression of P2Y 2 and P2Y 4 mRNA in mIMCD3. These data suggest that females have enhanced P2Y 2 and P2Y 4 -dependent regulation of Na + excretion in the renal medulla, compared to male and OVX rats, at least partially via an E 2 -dependent mechanism. This pathway may contribute to facilitated renal Na + handling in premenopausal females.

Background Epidemiological evidence supports an important association between air pollution exposure and hypertension. However, the mechanisms are not clear. Methods and Results Our present study found that long‐term exposure to fine particulate matter (PM 2.5 ) causes hypertension and impairs renal sodium excretion, which might be ascribed to lower D 1 receptor expression and higher D 1 receptor phosphorylation, accompanied with a higher G‐protein–coupled receptor kinase type 4 (GRK4) expression. The in vivo results were confirmed in in vitro studies (ie, PM 2.5 increased basal and decreased D 1 receptor mediated inhibitory effect on Na + ‐K + ATP ase activity, decreased D 1 receptor expression, and increased D 1 receptor phosphorylation in renal proximal tubule cells). The downregulation of D 1 receptor expression and function might be attributable to a higher GRK 4 expression after the exposure of renal proximal tubule cells to PM 2.5 , because downregulation of GRK 4 by small‐interfering RNA reversed the D 1 receptor expression and function. Because of the role of reactive oxygen species on D 1 receptor dysfunction and its relationship with air pollution exposure, we determined plasma reactive oxygen species and found the levels higher in PM 2.5 ‐treated Sprague‐Dawley rats. Inhibition of reactive oxygen species by tempol (4‐hydroxy‐2,2,6,6‐tetramethylpiperidin‐1‐oxyl) reduced blood pressure and increased sodium excretion in PM 2.5 ‐treated Sprague‐Dawley rats, accompanied by an increase in the low D 1 receptor expression, and decreased the hyperphosphorylated D 1 receptor and GRK 4 expression. Conclusions Our present study indicated that long‐term exposure of PM 2.5 increases blood pressure by decreasing D 1 receptor expression and function; reactive oxygen species, via regulation of GRK 4 expression, plays an important role in the pathogenesis of PM 2.5 ‐induced hypertension.

Purpose of review Current guidelines, based on extrapolations of observational studies or short-term relatively small clinical trials, recommend that daily sodium intake should be around 2 g/day or less. The assumption is that the relationship between sodium consumption and blood pressure (BP) levels is linear in all populations. Recent development suggests this may not be correct. We reviewed the literature on the association between sodium reduction and BP lowering, and preliminary data on 100,000 individuals from the Prospective Urban Rural Epidemiology study on sodium excretion and the association of sodium excretion with BP in general populations from 17 countries in five continents, with a focus on major subgroups. Recent findings Earlier observational studies have shown inconsistencies in their findings which were not addressed by the recommendations. The PURE results showed that associations between sodium intake and BP were not linear; proportionally, higher BP was found in individuals with higher sodium intake compared with those with lower sodium intake, in individuals with hypertension compared to those without hypertension, and in older individuals compared with younger individuals. Summary Recent data do not support the recommendation that all populations should reduce their sodium intake to one low level.

Although 24-h urinary measure to estimate sodium and potassium excretion is the gold standard, it is not practical for large studies. We compared estimates of 24-h sodium and potassium excretion from a single morning fasting urine (MFU) using three different formulae in healthy individuals.We studied 1083 individuals aged 35-70 years from the general population in 11 countries. A 24-h urine and MFU specimen were obtained from each individual. A subset of 448 individuals repeated the measures after 30-90 days. The Kawasaki, Tanaka, and INTERSALT formulae were used to estimate urinary excretion from a MFU specimen.The intraclass correlation coefficient (ICC) between estimated and measured sodium excretion was higher with Kawasaki (0.71; 95% confidence interval, CI: 0.65-0.76) compared with INTERSALT (0.49; 95% CI: 0.29-0.62) and Tanaka (0.54; 95% CI: 0.42-0.62) formulae (P 0.001). For potassium, the ICC was higher with the Kawasaki (0.55; 95% CI: 0.31-0.69) than the Tanaka (0.36; 95% CI: -0.07 to 0.60; P 0.05) formula (no INTERSALT formula exists for potassium). The degree of bias (vs. the 24-h urine) for sodium was smaller with Kawasaki (+313 mg/day; 95% CI: +182 to +444) compared with INTERSALT (-872 mg/day; 95% CI: -728 to -1016) and Tanaka (-548 mg/day; 95% CI: -408 to -688) formulae (P 0.001 and P = 0.02, respectively). Similarly for potassium, the Kawasaki formula provided the best agreement and least bias. Blood pressure correlated most closely and similarly with the 24-h and Kawasaki estimates for sodium compared with the other two formulae.In a diverse population, the Kawasaki formula is the most valid and least biased method of estimating 24-h sodium excretion from a single MFU and is suitable for population studies.

Objective: Recent GWAS studies found uromodulin gene polymorphisms to be associated with increased risk for hypertension (HT) and chronic kidney disease. It was hypothesized that relation of uromodulin with HT might be through effects on sodium renal excretion. Our aim was to analyse association of urinary uromodulin concentrations (uUMc) with blood pressure (BP) and sodium excretion in a group of untreated middle-aged subjects. Design and method: In this cross-sectional study 175 apparently healthy untreated subjects without a history for CV and with eGFR> 60 ml/min/1.73 m2 were enrolled. Fasting blood and urine 24-hour urine sample were obtained and BP was measured following ESH/ESC guidelines in office (Omron M6) and during regular working (ABPM: Mobile-O-Graph). Based on office BP subjects were divided according to the JNC-7 classification. Uromodulin was determined by Enzyme

Objective: It is empirically aware that inter-individual differences exist in sensitivity of salt taste. It is assumed that person with reduced sensitivity to salt taste may consume a higher amount of salt than those with a normal sensitivity of salt. The objective of this study is to reveal the relationship between the sensitivity of salt taste and salt intake. Design and method: In this study, we defined salt taste sensitivity by the threshold of the sense of salt taste. Therefore, we defined as reduced sensitivity when individuals were unable to sense salt taste in the concentration that majority of individuals could. Japanese residents who came to annual health checkups were recruited to this study. A series of salt-impregnated taste strips were used to measure salt taste intensity. Each taste strip was impregnated with sodium chloride at concentrations of 0, 0.6, 0.8, 1.0, 1.2, 1.4 and 1.6 g/cm 2 . Daily sodium intake was estimated from sodium excretion in the spot urine using Tanaka’s equation. Results: Among 1,207 participants, 979 (81.1%) individuals were considered to bear normal sensitivity because they were able to detect salt taste by taste strip of 0.6 or 0.8 g/cm 2 . However, 67 (5.6%) individuals were categorized as reduced sensitivity group because they were able to detect it only by the taste strip with the highest amount of salt, or unable to detect salt taste. Daily salt intake of reduced sensitivity group was significantly higher than those in normal sensitivity group (10.3g vs 9.7g, p Conclusions: Our study revealed the sensitivity of salt taste is associated with daily salt intake, even adjusted by gender and age. Strict reduction of salt is recommended especially for Smokers or persons with diabetes mellitus, not only because low BP recommendation but also they might pretend to consume salt because of reduced sensitivity of salt taste.

Objectives:Sodium intake is rarely monitored in clinical practice although it has been associated with blood pressure and antihypertensive drugs. 24-hour urine collection for sodium excretion is the most reliable method in estimating sodium intake, but the method is rather cumbersome. Thus this stud

Introduction: National efforts toward reducing population sodium intake necessitate developing a feasible and valid monitoring method, especially for the distribution tails given about 90% of the US population consumes more sodium than recommended. Objective: We developed and tested the validity of a statistical approach using one or two timed-spot urines to estimate population distribution of usual 24-hour sodium excretion. Methods: A convenience sample of 407 adults, 18-39 years of age, (54% female, 48% black) collected urine for a 24-hour period, placing each void in a separate container. Of these, 133 repeated the procedure 4-11 days later. Four timed-spot specimens (morning, afternoon, evening, and overnight) were selected from each 24-hour collection. We developed gender-specific equations using Fuller’s error-in-the-equation measurement error model to calibrate total sodium excreted in each of the one-spot (e.g., morning) and combined two-spot (e.g., morning + afternoon) urines to 24-hour sodium excretion. The calibrated sodium excretions were used to estimate the population distribution of usual 24-hour sodium excretion. Participants were then randomly assigned to modeling (n=160) or validation (n=247) groups to examine the bias in estimated population percentiles. Results: Median bias in predicting the 5 th , 25 th , 50 th , 75 th , and 95 th population percentiles of usual 24-hour sodium excretion with one-spot urine ranged from -367 to 284 mg (-7.7 to 12.2% of the observed usual excretions) for men and -604 to 486 mg (-14.6 to 23.7%) for women, and with two-spot urines from -338 to 263 mg (-6.9 to 10.4%) and -166 to 153 mg (-4.1 to 8.1%), respectively. Four of the six two-spot urine combinations produced no significant bias in predicting selected percentiles. Conclusions: Our approach to estimate the population distribution of usual 24-hour sodium excretion using calibrated spot urine sodium accounted for day-to-day variation and covariance between measurement errors, and produced percentile estimates with relatively low biases across low to high sodium levels. This may provide a low-burden, low-cost alternative to 24-hour collections in monitoring population sodium intake among healthy young adults and merits further investigation in other population subgroups.

We welcome further discussion of our article on sodium and cardiovascular disease (CVD).1 The methodology used in analyzing the Trials of Hypertension Prevention (TOHP) follow-up in the current article was prespecified. For those in the active sodium intervention, levels of sodium changed over time, and for some reflected short-term compliance with the intervention. Average sodium excretion would not reflect long-term usual intake for these participants and would introduce error. For this reason, we conducted our analysis solely among those who were not assigned to a reduced sodium intervention. In addition, as Drs Cohen and Alderman acknowledge,2 we previously found a 25% lower rate of CVD in the sodium reduction arms in an analysis that …

OBJECTIVES To assess the influence of sodium intake on the two components of arterial blood pressure [mean blood pressure (MBP) and pulse pressure] and left ventricular mass (LVM) in normotensive subjects and never-treated hypertensive patients. METHODS Blood pressure, LVM (M-mode echocardiography) and sodium excretion as an index of dietary sodium were measured in 459 males and 396 females, aged 14-93 years, with elevated (63% of population) or normal blood pressure. RESULTS Because pulse pressure decreased with age up to approximately 40 years of age, and increased thereafter, analysis was undertaken separately in 438 young (age < or = 40 years) and 417 middle-aged to elderly subjects. Before age 40 years, only pulse pressure was independently and positively influenced by urinary sodium excretion. After age 40 years, MBP and LVM index but not pulse pressure were positively influenced by urinary sodium excretion. When men and women were analysed separately according to tertiles of urinary sodium excretion, pulse pressure adjusted for MBP and age increased from the first to the third tertile of urinary sodium excretion in males (P < 0.03), but not in females. CONCLUSIONS The influence of sodium intake on pulse pressure was found in the younger subjects of both males and females and only in men older than 40 years.

Recent developments have led to renewed interest in the mechanisms that mediate the changes in sodium excretion in response to changes in arterial pressure, a phenomenon termed pressure-natriuresis. Pressure-natriuresis occurs in the absence of changes in filtered load and thus, the changes in sodium excretion are caused by changes in net tubular sodium reabsorption. Both proximal and distal nephron segments have been implicated as the sites of altered reabsorption. The specific mechanism responsible for pressure-natriuresis remains unresolved. One proposal suggests that changes in renal interstitial fluid pressure which may be due, in part, to a less efficient autoregulation of the renal medullary circulation than of the cortex, alter sodium reabsorption. Alternatively, recent studies indicate that increases in arterial pressure increase endothelial nitric oxide formation which inhibits sodium reabsorption via direct effects on the tubules as well as hemodynamically mediated effects.

Thank you for your interest in our recent article, “Testosterone Supplementation in Male Obese Zucker Rats Reduces Body Weight and Improves Insulin Sensitivity But Increases Blood Pressure.”1 Thank you also for your suggestions and for sharing the information from your human studies showing the negative correlation between sodium excretion and total testosterone in your hypertensive cohort.2 Unfortunately, we did not measure sodium excretion in these studies.1 The rats were in sodium balance, so the …

We thank Coelho Ortega et al1 for their comments on our article.2 As mentioned by the authors of the letter, little is known about the mechanisms associated with the reproducibility of the circadian blood pressure (BP) pattern, and even less is known about the reproducibility of the circadian pattern of sodium excretion. According to their observation, subjects who changed their dipping pattern from a dipper to a nondipper profile …

The interaction of sodium sensitivity and stress-induced cardiovascular reactivity was studied in white and black young adults aged 18-23 years. The cardiovascular response to difficult mental arithmetic was measured before and after 14 days of oral sodium loading (10 g NaCl/day added to the usual diet). A sodium-sensitive blood pressure response occurred in 18.4% of whites and 37.3% of blacks. A significant correlation between blood pressure change and sodium excretion occurred in the sodium-sensitive group (r = - 0.28, p less than 0.01). High sodium intake did not augment blood pressure or heart rate response to the beta-adrenergic-mediated stimulus of mental arithmetic in the population, which was grouped by blood pressure, race, or sodium sensitivity.

The study by Alderman et al1 in the current issue of Hypertension provides data that raise a question of whether a decrease in sodium intake lowers risk of cardiovascular disease. The National High Blood Pressure Education Program Working Group2 cited a reduction in sodium intake as one of the most effective approaches to preventing hypertension. They recommend a multifaceted approach to public education that includes limiting excess sodium intake as a key element. The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure3 recommends lifestyle modifications, including sodium reduction, as a first-line treatment for mildly and moderately hypertensive individuals. Much of the evidence concerning the benefit of a decrease in sodium intake is derived from studies of blood pressure. Observational data, from both between-population and within-population studies4 5 and particularly data from the INTERSALT study,6 7 show a consistent direct relationship of sodium excretion (UNaV) to blood pressure. Current estimates from INTERSALT7 suggest a 100-mmol decrease in sodium is associated with a decrease in systolic pressure of 3.1 mm Hg. Randomized trial data have generally supported these observational results.8 9 The recent Trials of Hypertension Prevention, Phase I10 found that decreases in systolic/diastolic pressures of 1.7/0.9 mm Hg were associated with average sodium decreases of about 44 mmol/24 h, a finding comparable to other trials among normotensive subjects.9 The results in trials among hypertensive subjects tend to be even stronger. An overview9 suggests decreases in systolic/diastolic pressures of 4.9/2.6 mm Hg in trials among …

OBJECTIVE Renal responses of anaesthetized Milan hypertensive (MHS) and Milan normotensive (MNS) rats to des-[Glu18-Ser19-Gly20-Leu21-Gly22]r atrial natriuretic peptide-4-23 (cANP4-23) a specific ligand for atrial natriuretic petide (ANP) clearance receptors were examined. METHODS The peptide was administered intravenously as an initial bolus injection (10 micrograms/kg body weight) followed by constant infusion (1 microgram/min per kg body weight) for 30 min. Glomerular filtration rate, urine flow, sodium excretion and mean blood pressures were measured. Using the same protocol, plasma ANP levels were determined. RESULTS Plasma ANP levels were significantly increased in both Milan strains (from 9.5 +/- 1.8 to 23.7 +/- 3.2 fmol/ml in MHS rats and from 9.8 +/- 1.2 to 15.9 +/- 1 fmol/ml in MNS rats). This increase was significantly greater in the MHS than in the MNS rats. The cANP4-23 infusions were diuretic and natriuretic in both strains of rats but despite a greater rise in plasma ANP level, the renal response was attenuated in the MHS compared with that in the MNS rats. Furthermore, the time course differed in that the hypertensive rats had a diuresis of slower onset. During cANP4-23 infusion, the mean blood pressure decrease was greater in the MHS rats, consistent with the fact that phenylephrine-precontracted isolated MHS rat aortae were threefold more sensitive to ANP-induced relaxation than were MNS rat aortae. Displacements of [125l]-rANP by rANP and cANP4-23 in isolated renal glomeruli indicated that MHS rats have similar amounts of cANP receptors but with a higher affinity for cANP than have MNS rats. CONCLUSION cANP4-23 infusion increased plasma ANP more in MHS than in MNS rats. Renal responses were attenuated in the MHS rat compared with those in MNS rats. These differential actions cannot be explained in terms of glomerular ANP receptor densities, although aortic ring sensitivities differ between the two strains of rat.

This study explored the association between sodium excretion and blood pressure (BP). A new method was used to minimize the measurement error introduced by the large intrinsic variability of 24-hour sodium excretion. The ratio of intra- to interindividual variation was used to estimate the number of measurements needed to characterize the individual. When seven consecutive 24-hour samples were collected from 73 children, ages 11-14 years, a significant correlation between mean individual sodium excretion and BP was demonstrated. The independent relationship persisted when controlling for height, weight, pulse, age, sex and race (p = 0.045), but was eliminated by simultaneously considering mean creatinine excretion. Although the cross-sectional association described is quantitatively weak, a linear relationship between BP and sodium over the range consumed in this society could be important for prevention.

To evaluate the role of altered efferent renal sympathetic nerve activity in the exaggerated natriuresis of the spontaneous hypertensive rat (SHR), we measured efferent renal sympathetic nerve activity in anesthetized age- and sex-matched SHR and normotensive Wistar Kyoto (WKY) control rats during control and intravenous saline volume expansion. Mean arterial pressure was 40-60 mm Hg higher in SHR than in WKY. During volume expansion, the increment in urinary flow rate (17.5 +/- 3.1 vs 42.8 +/- 8.0 microliters/100 g/min) and sodium excretion (8.1 +/- 1.5 vs 15.2 +/- 2.3 muEq/min) were greater in SHR than in WKY. During control, efferent renal sympathetic nerve activity was 12.2 +/- 0.4 Hz in WKY and 12.0 +/- 0.5 Hz in SHR and fell equally during volume expansion to 5.0 +/- 0.6 Hz in WKY and to 4.0 +/- 0.8 Hz in SHR. Thus, these studies demonstrate that the exaggerated natriuresis of SHR as compared to WKY cannot be attributed to differences in reflex withdrawal of renal sympathetic nerve activity.

Previous studies have shown that vasopressin potentiates the natriuresis produced by atriopeptin. In five anesthetized dogs of this study, we found that the potentiation was proportional to the dose of vasopressin infused. Sodium excretion was 46 +/- 16 mueq/min with atriopeptin (103-126) (AP24) alone (0.36 nmol/kg.min), was increased to 127 +/- 29 by concomitant intravenous infusion of 0.4 mU/kg.min vasopressin, was further increased to 301 +/- 75 by 1.2 mU/kg.min vasopressin and leveled off at 328 +/- 37 with 3.6 mU/kg.min vasopressin. To investigate whether the potentiation by vasopressin was due to an intrarenal action, we infused three doses of vasopressin (0.04, 0.12, and 0.36 mU/kg.min) into the renal artery during intravenous AP24 infusion in a second group of five dogs. The natriuresis, 128 +/- 18 mueq/min, was unaffected by any intrarenal dose of vasopressin. In a third group, we determined whether the potentiation produced by vasopressin was mediated by a mechanism involving the renal nerves by denervating the left kidney before AP24 infusion. In the denervated kidneys, sodium excretion was increased from a control value of 33 +/- 5 mueq/min to 303 +/- 38 with AP24 alone and was unresponsive to subsequent intravenous vasopressin administration. The exaggerated natriuresis with AP24 alone was of the same magnitude as that produced by AP24 plus the highest doses of intravenous vasopressin in the innervated kidneys of the first group. From these results we conclude that the potentiation of AP-induced natriuresis by vasopressin is mediated by a mechanism involving the renal nerves and probably results from the known effect of vasopressin to inhibit renal nerve activity.

How many 24-hour urine sodium measurements are adequate for characterizing a child's salt intake? Can overnight urine specimens accurately replace 24-hour collections for salt assessment? A sample of 73 6th-8th grade children was taken from two parochial schools in Chicago to investigate systematically these questions. Seven consecutive 24-hour-urine specimens were collected from each child. The estimated ratio of intra- to inter-individual variances was 1.94 for 24-hour-urine sodium. Based on this value, eight 24-hour specimens are necessary to limit to 10% the diminution of the estimated correlation coefficient between 24-hour-urine sodium and blood pressure. Six measurements are required to reduce to 0.01 the probability of misclassifying a child in tertile 1 versus tertile 3. The overnight specimens show a moderate consistency with the 24-hour collections in detecting children with high or low salt intake. For example 92% and 85% of children in the fifth quintile and the third tertile respectively of the true mean overnight sodium have their true mean 24-hour Na in the upper half of the distribution. These results suggest that in a large scale epidemiologic study, overnight specimens may be reasonable alternatives when 24-hour-urine sodium is practically very difficult to collect.

Blood pressure (BP) and associated factors were determined in 1737 men in a remote Kenyan agricultural community. Systolic BP showed no significant rise with age until after 54 years; diastolic BP showed a small rise with age. Both systolic and diastolic BP correlated with weight independent of age. Systolic and diastolic BP correlated positively with casual urinary sodium/potassium and negatively with potassium/creatinine ratios. Both systolic and diastolic BP correlated significantly with the number of years of education, as did urinary sodium/potassium and sodium/creatinine ratios. Potassium/creatinine ratios were negatively correlated with the number of years of education. Blood pressure and urinary sodium/creatinine ratios were significantly lower in subsistence farmers compared with those in other occupations, and potassium/creatinine ratios were significantly higher. Two pilot studies of Luo tribesmen showed a strong correlation between casual urinary electrolyte ratios and those derived from 24-hour urine samples and a greater variance of sodium excretion between these people than that found within individuals. These results suggest that a relationship between BP and casual urine electrolyte estimations may be identifiable in communities where there is less day-to-day dietary variation. They also suggest that some of the changes in BP associated with urbanization could be mediated by changes in dietary electrolytes.

Low-dose (0.025 micrograms/kg per min) noradrenaline infusion, resulting in a physiological plasma increment (280 pg/ml), was antinatriuretic in normal salt-replete male subjects. The reduction in sodium excretion (-20%, P less than 0.01) occurred without any change in the glomerular filtration rate but was associated with a significant (P less than 0.02) decline in lithium clearance. These results suggest that changes in circulating noradrenaline, within the physiological range, can decrease sodium excretion in man by enhancing proximal tubular sodium reabsorption. These findings extend previous investigations in man which used pharmacological doses of noradrenaline and are in agreement with animal evidence for a renal tubular antinatriuretic effect of the sympathetic nervous system.

The changes in extracellular fluid volume (ECV) in two groups of surgical patients, one receiving Ringer's lactate solution intraoperatively and the other receiving only dextrose and water, were assessed. A deficit in the ECV, as measured by radioactive sulfate, of 1.9 +/- 0.8 l (p less than 0.003) compared to the preoperative volume was found in the dextrose group. This was accompanied by a decrease in the mean creatinine clearance (-13% p less than 0.01), the mean urinary sodium excretion (-57% p less than 0.05), and the mean rate of clearance of the sulfate tracer (-18% p less than 0.01). The use of intraoperative Ringer's lactate (1660 cc +/- 96 cc) resulted in no change in the ECV, an increase in the mean creatinine clearance (+10% p less than 0.05), and no change in sodium excretion or tracer clearance. As a result of these findings, it appears that postoperative sodium retention is a physiologic response to a decreased ECV, which can be prevented by the administration of Ringer's lactate.

Nine well-motivated adults, knowledgeable about nutrition, kept food records, saved food portions equal to what had been eaten, and collected 24-hour urine samples for 3 consecutive days. Estimates of sodium and potassium intake were calculated from food table analyses of written food records and from flame photometric analyses of food portions. For each subject the mean of the estimates for each of the 3 days was compared with the mean of urine analyses for sodium and potassium for each of the 3 days. For the group of nine subjects, the average estimate of sodium intake from analyses of food records was 11% lower than the average estimate of urinary sodium excretion; the average estimate of sodium intake from analysis of food portions was 2% higher than urinary sodium excretion. For individuals, there were large differences between estimates of intake and measurement of sodium excretion. For the group of nine subjects, the average estimate of potassium intake from analysis of food records was less than 1% lower than the average estimate of potassium urinary excretion; the average estimate of potassium intake from analysis of food portions was 13% higher than potassium urinary excretion. For individuals, as with sodium, there were large differences between estimates of intake and measurement of potassium excretion.

s of Scientific Papers presented to the American Society of Anesthesiologists, 1969. Deutsch S., and others. Cyclopropane effects on renal function in normal man. Anesthesiology 28:547-558, May-June 1967. -. , and others. Changes in renin activity of peripheral venous blood during general anesthe- sia. Fed.Proc. 26:2, 1967. Given, Barbara, and Simmons, S. J. Castroenterol- ogy in Clinical Nursing. St. Louis, C. V. Mosby Co., 1975. Goodhart, R. S., and Shils, M. E., editors, Modem Nutrition in Health and Disease; Dietotherapy. fifth edition, Phila., Lea & Febiger, 1973. Mazze, R. I., and Barry, K. G. Prevention of functional renal failure during anesthesia and surgery of sustained hydration and mannitol infusion. Anesth.Analg. 46:61-68, Jan.-Feb. 1967. Metheny, N. M., and Snively, W. D., Jr. Nurses' Handbook of Fluid Balance. 2d ed. Philadelphia, J. B. Lippincott Co., 1974. Moore, F. D. Metabolic Care of the Surgical Patient. Philadelphia, W. B. Saunders, 1959. Moyer, C. A. Fluid Balance. Chicago, Year Book Publishers, 1952. Pezzi, P., and others. Methoxyflurane and renal toxicity. Lancet 1:827, 1966. Randall, R. E., Jr., and Papper, S. Mechanism of postoperative limitation in sodium excretion: the role of extracellular fluid volume and of adrenal cortical activity. J.Clin.Invest. 37:1628- 1641, Nov. 1958. Snively, W. D., Jr., and Beshear, D. R. Textbook of Pathophysiology. Philadelphia, J. B. Lippincott Co., 1972. American Journal of Nursing/May 1978 845 This content downloaded from 157.55.39.144 on Wed, 07 Sep 2016 04:37:11 UTC All use subject to http://about.jstor.org/terms

In healthy young subjects the sodium excretion is decidedly less in the sitting than in the recumbent posture. The difference can be partially overcome by compression of the neck in the sitting position. Some possible implications of these observations will be considered in the subsequent communications.

During the initial phase of decline in cardiac output following the administration of digitoxin to normal subjects, sodium excretion did not decline. Several days later, as cardiac output rose toward the normal level, sodium output decreased in most subjects. The possible implication of these re sults in relation to the regulation of sodium excretion is discussed.

Pyrogen, when administered intravenously to normotensive and hypertensive men, produced initially vasoconstriction and subsequently marked renal vasodilatation, both resulting from direct effects on the renal vasculature. The absolute renal plasma flow, both during control observations and at the height of renal hyperemia, was greater in normotensives, but the percentage change was greater in hypertensive subjects. Extraction of p -aminohippurate diminished during renal hyperemia. Medullary renal plasma flow was higher in normotensive subjects both during control observations and at the height of renal hyperemia. Simultaneously with the development of renal hyperemia, sodium excretion increased without alterations in filtered load of sodium and was prompt in its development in normotensives and delayed in hypertensives. This is attributed to a transient, small, yet probably significant decrease in filtered load of sodium during vasoconstriction immediately following the administration of pyrogen. Simultaneously with the development of renal hyperemia, there was in both groups an increase in solute excretion and tubular reabsorption of solute-free water.