Variations In Sodium Intake Research Articles

Wood and meat as complementary sources of sodium for Kanyawara chimpanzees (Pan troglodytes).

Sodium, a vital micronutrient that is often in scarce supply for tropical herbivores, is sometimes found at high concentration in decaying wood. We tested two hypotheses for chimpanzees: first, that wood-eating facilitates acquisition of sodium; second, that wood-eating occurs in response to the low availability of sodium from other dietary sources. We studied the behavior of more than 50 chimpanzees of all age-sex classes in the Kanyawara community of Kibale National Park, Uganda. We quantified the sodium content of dietary items, including wood samples from tree species that chimpanzees consumed or did not consume. To assess variation in sodium intake, we used 7 years of data on time spent feeding on plant foods, 18 months of data on rates of food intake by adult females, and 20 years of data on meat-eating. Major dietary sources of sodium were wood, fruits and meat. Chimpanzees consumed wood primarily from decaying trees of Neoboutonia macrocalyx (Euphorbiaceae), which had substantially higher sodium content than all other dietary items tested. Wood-eating was negatively correlated with fruit-eating. Females ate wood more often than males, while males had a greater probability of consuming meat at predation events. We propose that females ate wood more often than males because females had reduced access to meat, their preferred source of sodium. This hypothesis suggests that the need for sodium is a motivating reason for chimpanzees to consume both meat and wood.

Variation in Sodium Intake and Intra-individual Change in Blood Pressure in Chronic Kidney Disease

In the kidney disease clinic setting, higher-than-usual blood pressure is often ascribed to recent dietary sodium indiscretion. While clinical trials demonstrate a clear relationship between salt intake and blood pressure on the population level, it is uncertain whether real-world variation in sodium intake within individual chronic kidney disease (CKD) patients is associated with fluctuations in blood pressure. We analyzed data from the Phosphorus Normalization Trial, in which participants with CKD eating their usual diets completed at least three 24-hour urine collections over 9months, from which we measured sodium. Blood pressure was measured at the time of 24-hour urine collections. For each individual participant, we assessed the slope of the relationship between sodium intake and mean arterial blood pressure (MAP). Among 119 participants (mean age 67years and mean estimated glomerular filtration rate 31mL/minute/1.73m2), there was substantial variation in sodium intake as measured by 24-hour urine collections (mean intake 3,903mg/day, standard deviation 1037mg/day). Individual participants had highly variable associations between their sodium intake and their MAP; 47% (n=56) had inverse associations between sodium and MAP, whereas the remainder had positive (salt-sensitive) associations. Among CKD patients, there is substantial variation in sodium intake but no predictable relationship between dietary sodium and blood pressure in individuals. The frequent dismissal of elevated blood pressure readings as related to recent sodium intake in clinic may be a misapplication of large-scale population data to explain individual variability and may contribute to clinical inertia regarding high blood pressure treatment.

Perceived 6-n-Propylthiouracil (PROP) Bitterness Is Associated with Dietary Sodium Intake in Female Japanese College Students.

Despite the negative health consequences of a high sodium consumption, humans consume well above the recommended levels. This study examines whether or not the dietary intake of sodium was affected by individual variation of the perceived bitterness of 6-n-propylthiouracil (PROP), and examines the relationship between the perceived bitterness of PROP and the preferred NaCl concentration of broth. Female students (20-22 y old) were recruited from the university community. Genotypes of A49P and I296V polymorphism of the TAS2R38 bitter taste receptor were determined for each subject. Samples containing NaCl, PROP or broth in 5-mL portions were evaluated by sensory testing. The participants completed a food record for each diet. Our results indicate that the individuals perceiving PROP to be more bitter had consumed a greater amount of dietary sodium. In contrast, there was no significant positive correlation between an individual's perceived saltiness and the dietary sodium intake. Those who perceived PROP to be more bitter preferred a broth containing a higher concentration of NaCl. All of these correlations were apparent even after those subjects with TAS2R38 AI/AI homozygotes (PROP non-taster) had been excluded. In conclusion, the results of this study suggest that a factor affecting the bitter rating of PROP other than the AI/AI homozygotes of TAS2R38 contributes to the variation in sodium intake and the preference for salty food.

Sodium Intake, Dietary Knowledge, and Illness Perceptions of Controlled and Uncontrolled Rural Hypertensive Patients

Introduction and Objectives. Nutritional knowledge of the patients is important in dietary adherence. This study aimed to determine the relationship between illness perceptions and nutritional knowledge with the amounts of sodium intake among rural hypertensive patients. Methods. In a cross-sectional study, 671 hypertensive patients were selected in a multistage random sampling from the rural areas of Ardabil city, Iran, in 2013. Data were collected using a questionnaire consisting of four sections and were analyzed using Pearson correlation and multiple linear regressions by SPSS-18. Results. The mean of sodium intake in the uncontrolled hypertensive patients was 3599 ± 258 mg/day and significantly greater than controlled group (2654 ± 540 mg/day) (P < 0.001). Knowledge and illness perceptions could predict 47.2% of the variation in sodium intake of uncontrolled group. A significant negative relationship was found between knowledge and illness perceptions of uncontrolled hypertensive patients with dietary sodium intake (r = −0.66, P < 0.001 and r = −0.65, P < 0.001, resp.). Conclusion. Considering the fact that patients' nutritional knowledge and illness perceptions could highly predict their sodium intake, the importance of paying more attention to improve patients' information and perceptions about hypertension is undeniable, especially among the uncontrolled hypertensive patients.

Renal hemodynamic effects elicited by acute cyclooxygenase-2 inhibition are not related to angiotensin II levels

numerous studies have demonstrated that cyclooxygenase-2 (COX-2) is involved in the regulation of renal function. It has also been shown that renal COX-2 expression and activity change in response to physiological stimuli, such as variations in sodium intake, and in response to changes in several

Reduced nephron endowment due to fetal uninephrectomy impairs renal sodium handling in male sheep

Reduced nephron endowment is associated with development of renal and cardiovascular disease. We hypothesized this may be attributable to impaired sodium homoeostasis by the remaining nephrons. The present study investigated whether a nephron deficit, induced by fetal uninephrectomy at 100 days gestation (term=150 days), resulted in (i) altered renal sodium handling both under basal conditions and in response to an acute 0.9% saline load (50 ml.kg-1 of body weight.30 min-1); (ii) hypertension and (iii) altered expression of renal channels/transporters in male sheep at 6 months of age. Uninephrectomized animals had significantly elevated arterial pressure (90.1+/-1.6 compared with 77.8+/-2.9 mmHg; P<0.001), while glomerular filtration rate and renal blood flow (per g of kidney weight) were 30% lower than that of the sham animals. Total kidney weight was similar between the groups. Renal gene expression of apical NHE3 (type 3 Na+/H+ exchanger), ENaC (epithelium Na+ channel) beta and gamma subunits and basolateral Na+/K+ ATPase beta and gamma subunits were significantly elevated in uninephrectomized animals, while ENaC alpha subunit expression was reduced. Urine flow rate and sodium excretion increased in both groups in response to salt loading, but this increase in sodium excretion was delayed by approximately 90 min in the uninephrectomized animals, while total sodium output was 12% in excess of the infused load (P<0.05). In conclusion, the present study shows that animals with a congenital nephron deficit have alterations in tubular sodium channels/transporters and cannot rapidly correct for variations in sodium intake probably contributing to the development of hypertension. This suggests that people born with a nephron deficit should be monitored for early signs of renal and cardiovascular disease.

Estimation of 24‐Hour Sodium Excretion from Spot Urine Samples

Despite the effects of sodium intake on blood pressure and on response to antihypertensive medication, sodium intake is rarely monitored in clinical practice. The current method, the 24-hour urine collection for sodium excretion, is cumbersome, often incorrectly performed, and not commonly ordered. Further, its results have limited meaning because of the substantial day-to-day variation in sodium intake. A spot urine test to enable convenient, inexpensive, and serial monitoring of sodium excretion would be desirable. In this study, the accuracy of predicting 24-hour sodium excretion from a spot urine sample was assessed. The urine sodium/creatinine ratio was determined from the following urine samples: an "AM sample," submitted at the beginning of the 24-hour urine collection; a "PM sample" collected in the later afternoon/early evening before dinner, at roughly the midpoint of the collection; and a "random sample," collected after its completion. The ratio was then corrected for 24-hour creatinine excretion. The strongest correlation between predicted and actual 24-hour sodium excretion was observed with the PM sample collected near the midpoint (r=0.86, P<.001). This sample also identified persons with sodium excretion <100 mEq/d with a sensitivity of 100% and specificity of 82%. The sodium/creatinine ratio from a spot urine sample collected in the late afternoon/early evening at roughly the midpoint of the 24-hour collection, and adjusted for 24-hour creatinine excretion, strongly correlated with 24-hour sodium excretion. Additional studies are merited to further evaluate the role of the spot urine sample in assessing sodium intake.

Decreased cortisol production in male type 1 diabetic patients.

It is unclear whether cortisol production and the 11betaHSD-mediated cortisol to cortisone interconversion are different between type 1 diabetic patients and healthy subjects. Fourteen male, nonobese, normotensive type 1 diabetic patients without severe complications (HbA1c < 8.5%) were studied twice during a daily sodium intake of 50 and 200 mmol, and were then compared with 14 individually matched healthy subjects. Cortisol production was assessed by the sum of urinary cortisol metabolite excretion. Urinary ratios of (tetrahydrocortisol + allo-tetrahydrocortisol)/tetrahydro-cortisone [(THF + allo-THF)/THE] and of free cortisol/free cortisone [UFF/UFE] were determined as parameters of 11betaHSD activity. Sum of urinary cortisol metabolite excretion during low- and high-salt diet was 7.4 +/- 2.5 vs. 7.7 +/- 2.3 nmol min-1 m-2 (NS) in diabetic patients and 9.7 +/- 2.1 vs. 11.2 +/- 4.1 nmol min-1 m-2 (NS) in healthy subjects, respectively (P < 0.05 vs. healthy subjects at both diets). The allo-THF excretion and allo-THF/THF ratios were lower in the diabetic than in the healthy males during both diets (P < 0.05). Urinary (THF + alloTHF)/THE and UFF/UFE were similar in both groups and remained unchanged after salt loading. The sum of urinary cortisol metabolite excretion as a measure of cortisol production is lower in nonobese, normotensive type 1 diabetic males with adequate glycaemic control and without severe complications, irrespective of sodium intake. We suggest that this is at least in part as result of diminished 5alpha reductase activity, resulting in a decreased cortisol metabolic clearance. In type 1 diabetic and in healthy males, the 11betaHSD setpoint is not affected by physiological variations in sodium intake.

Effects of sodium intake on cardiovascular variables in humans during posture changes and ambulatory conditions.

The hypothesis was tested that cardiac output (CO) and stroke volume (SV) are increased by a moderate physiological elevation in sodium intake with a more pronounced effect in the ambulatory upright seated than supine position. Fourteen healthy males were investigated during ambulatory and controlled laboratory conditions at the end of two consecutive 5-day periods with sodium intakes of 70 (low) and 250 (high) mmol/24 h or vice versa, respectively. Comparing high and low sodium intake, plasma volume and plasma protein concentrations were 9 and 8% higher in the seated and the supine position, respectively. When seated during laboratory conditions, CO was 5.3 +/- 0.2 l/min on the high sodium intake vs. 4.8 +/- 0.2 l/min on the low (P < 0.05), and SV was 81 +/- 3 vs. 68 +/- 3 ml (P < 0.05). In the supine position, SV was 107 +/- 3 ml on the high vs. 99 +/- 3 ml (P < 0.05) on the low sodium intake, while CO remained unchanged. The difference in CO and SV induced by the change in sodium intake was significantly higher in the seated than in the supine position (P < 0.05). During upright ambulatory conditions, CO was 5.9 +/- 0.2 l/min during the high and 5.2 +/- 0.2 l/min during the low sodium intake (P < 0.05), and SV was 84 +/- 3 and 69 +/- 3 ml (P < 0.05), respectively. Mean arterial pressure was unchanged by the variations in sodium intake. In conclusion, increments in sodium intake within the normal physiological range increase CO and SV and more so in the seated vs. the supine position. These changes are readily detectable during upright, ambulatory conditions. The results indicate that the higher SV and CO could constitute an arterial baroreflex stimulus for the augmented renal sodium excretion.

The effect of sodium supplementation on glucose tolerance and insulin concentrations in patients with hypertension and diabetes mellitus

Severe short-term sodium restriction or extreme sodium loading may alter glucose tolerance and insulin resistance in patients with hypertension, but it is unclear whether variations in sodium intake within the clinically observed range affect glucose tolerance. To examine this issue, 21 patients with primary hypertension with average sodium excretion of 116 ± 55 mEq/day were randomized to consecutive 4-week periods of placebo therapy and sodium chloride supplementation 2 g four times a day in a single-blind crossover study design. A 75-g oral glucose tolerance test (GTT) with simultaneous insulin levels was performed at the end of each intervention period. For the group as a whole, urinary sodium excretion increased on sodium chloride to 267 ± 118 mEq/day versus control (placebo) phase of 135 ± 53 mEq/day, P < .001. Total glycemic response in the oral GTT (area under the glucose curve) was 8.0% lower during sodium supplementation, P < .001. Secondary analysis revealed that the effect of sodium was noteworthy in 1) type 2 diabetic subjects ( n = 8), 2) sodium-sensitive subjects ( n = 10), and 3) nondiabetic subjects receiving antihypertensive drug treatment ( n = 6). The total insulinemic response to oral GTT was also lowered by sodium loading among diabetic subjects. Thus, an abundant sodium intake may improve glucose tolerance and insulin resistance, especially in diabetic, salt-sensitive, and or medicated essential hypertensive subjects.

Morphological adaptations to induced changes in transepithelial sodium transport in chicken lower intestine (coprodeum): a study of resalination, aldosterone stimulation, and epithelial turnover.

Transepithelial sodium transport and epithelial morphology during short-term adaptation to resalination or aldosterone stimulation were studied in the chicken coprodeum. Coprodeum was sampled for light and electron microscopy after 0-3 days of resalination in hens on a low-NaCl diet and after 0-6 days of aldosterone stimulation in hens on a high-NaCl diet. Sodium transport was measured in vitro with Ussing chambers. Plasma osmolality and electrolyte concentrations were measured in aldosterone-stimulated hens. Epithelial proliferation and migration between 1 h and 16 days were investigated in chickens on high-NaCl and low-NaCl diets using a bromodeoxyuridine technique. Resalination abolished the otherwise high sodium transport within 1 day, while the height and number of microvilli, as well as the number of brush cells, decreased over 3 days. Aldosterone stimulation increased sodium transport, the height and number of microvilli, and the brush-cell number. Bromodeoxyuridine studies indicated an epithelial cell turnover of more than 16 days. The results thus demonstrate that epithelial cells have an unusual capacity to adjust rap- idly to variations in sodium intake. A strong correlation between structure and function was apparent.

Effect of dopamine2 blockade on renal function under varied sodium intake.

This study explored the role of the dopamine-2 receptor (DA2) in the control of renal blood flow (RBF) and the influence of variations in sodium intake. These relationships have not been previously defined in man. Seven normotensive male subjects underwent a low dose dopamine (DA) infusion (1 microgram/kg.min) for 3 h, known to activate both DA1 and DA2 receptors. The effect of DA2 receptor on renal hemodynamics was studied using a relatively specific DA2 blocker [domperidone (DOM); 60 mg, orally] alone and with a DA infusion. Systemic and renal hemodynamics parameters were measured noninvasively. Urinary prostacyclin was measured in 3-h urine specimens, obtained during the DA infusion. The DA infusion increased RBF and prostacyclin during both normal and high salt diets, but this effect was attenuated on a low salt diet. DOM alone significantly reduced basal RBF during normal (1304 +/- 48 vs. 1175 +/- 45 mL/min.1.73 m2; P < 0.01) and low salt diets (1402 +/- 80 vs. 1220 +/- 101 mL/min.1.73 m2; P < 0.02), but was without effect during high sodium intake. DOM had no effect on prostacyclin excretion at any level of salt intake. These results suggest that both DA1 and DA2 are activated in renal vessels by DA, and that DA2 receptors play a role in the renal vasodilating action of DA. Changes in sodium balance alter the actions of the two receptors (DA1 and DA2) in a coordinated fashion in the regulation of RBF.

Effects of Variation in Sodium Intake on Cystinuria

This study was designed to characterize the effect of urinary sodium excretion on amino acid excretion in cystinuria. We studied three homozygous patients with cystinuria at various levels of sodium intake ranging between 50 and 230 mmol/day. A reduction in sodium intake produced a marked decrease in rates of urinary cysteine excretion. The low-sodium diet also reduced the excretion of lysine but had no significant effect on the excretion of ornithine or arginine. We conclude that a dietary restriction of sodium may reduce the urinary excretion of cystine and can provide a simple and safe long-term approach to the treatment of cystinuria.

Methodology of sodium sensitivity assessment. The example of age and sex.

This article addresses the methodology of sodium sensitivity assessment. There have been reports to suggest that a high sodium intake is a cause of elevated blood pressure and trials to indicate that a reduction in sodium intake may reduce blood pressure that is already high; the implications of these findings are discussed. Many studies on sodium sensitivity suffer from what could be called the "normal probability fallacy"; without appropriate control conditions, an intervention such as sodium restriction may incorrectly be assigned to a more pronounced response in a subgroup of the study population. As an example, findings are reviewed of age and sex as determinants of a response of blood pressure to variations in sodium intake. The limited data available suggest that subjects that are older and have higher blood pressure levels seem to benefit more from a reduction in sodium intake. In addition, elderly subjects at a high dietary sodium intake may have a higher risk of developing hypertension. Findings in both nonexperimental and experimental studies tend to support this view. Findings on sex differences are less consistent. A systematic approach to the assessment of factors and mechanisms responsible for sodium sensitivity in some subjects is needed to determine who might benefit most. Until more data are available, there is little basis to discriminate sodium-sensitive from sodium-resistant hypertensive subjects.

Observational studies of salt and blood pressure.

The observational data relating salt and blood pressure (excluding INTERSALT) are reviewed. Important methodological difficulties and biases are inherent to both across- and within-population studies and confuse their interpretation. Across-population studies are positive but rely on data drawn from the international literature based on a variety of unstandardized field methods; they are prone to unmeasured (ecological) confounding. Within-population studies generally lack statistical power and are subject to major regression-dilution bias (because of considerable day-to-day variation in sodium intake), which could conceal true correlations between sodium and blood pressure. Nevertheless, an overview of reported studies that used 24-hour urine excretion to quantify intake shows positive and highly significant correlations between sodium and blood pressure for both men and women and for systolic and diastolic blood pressures. These results are consistent with the INTERSALT findings and those from trials of sodium restriction.

Urinary Kallikrein Excretion in Response to Variations in Sodium Intake and Excretion

Conference Abstract| December 01 1985 Urinary Kallikrein Excretion in Response to Variations in Sodium Intake and Excretion A. Wright; A. Wright 1University of Southampton, Department of Medicine, St. Mary's Hospital, Portsmouth PO3 6AD. Search for other works by this author on: This Site PubMed Google Scholar S.K. Campbell; S.K. Campbell 1University of Southampton, Department of Medicine, St. Mary's Hospital, Portsmouth PO3 6AD. Search for other works by this author on: This Site PubMed Google Scholar J.D.M Albano; J.D.M Albano 1University of Southampton, Department of Medicine, St. Mary's Hospital, Portsmouth PO3 6AD. Search for other works by this author on: This Site PubMed Google Scholar A. Farrer; A. Farrer 1University of Southampton, Department of Medicine, St. Mary's Hospital, Portsmouth PO3 6AD. Search for other works by this author on: This Site PubMed Google Scholar J.G.B Millar J.G.B Millar 1University of Southampton, Department of Medicine, St. Mary's Hospital, Portsmouth PO3 6AD. Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1985) 69 (s12): 67P. https://doi.org/10.1042/cs069067P Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation A. Wright, S.K. Campbell, J.D.M Albano, A. Farrer, J.G.B Millar; Urinary Kallikrein Excretion in Response to Variations in Sodium Intake and Excretion. Clin Sci (Lond) 1 December 1985; 69 (s12): 67P. doi: https://doi.org/10.1042/cs069067P Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1985 The Biochemical Society and the Medical Research Society1985 Article PDF first page preview Close Modal You do not currently have access to this content.

Renal sodium handling in normal humans subjected to low, normal, and extremely high sodium supplies.

We studied renal sodium handling, extracellular fluid volume (ECFV), plasma renin activity, aldosterone and norepinephrine, and blood pressure in eight healthy volunteers after equilibration on intakes of 20, 200, and 1,128 +/- 141 meq sodium, respectively. Renal sodium handling was assessed by means of clearance studies during maximal water diuresis and lithium clearance. Urinary sodium excretions were 22 +/- 4, 202 +/- 19, and 1,052 +/- 86 meq/day. From the lower to the upper sodium intake level, 24-h creatinine clearance rose from 111 +/- 7 to 136 +/- 11 ml/min and inulin clearance from 103 +/- 9 to 129 +/- 9 ml/min, whereas proximal and distal fractional sodium reabsorption (FSRprox and FSRdist, respectively) fell from 86.8 +/- 1.3 to 79.0 +/- 2.7% and from 96.5 +/- 0.5 to 76.0 +/- 1.9%, respectively. During the normal sodium intake (200 meq), intermediate values were recorded. The changes in fractional lithium clearance were less consistent but correlated with FSRprox (r = 0.78, P less than 0.001) and not with FSRdist. Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. No consistent rise in blood pressure was detected. These observations indicate that in healthy humans renal adaptation to vast variations in sodium intake includes resetting of glomerular filtration rate, FSRprox, and, in particular, FSRdist. Alterations in neurohumoral factors may play a dominant role in this adaptation.

Steroidogenic properties of a new aldosterone-stimulating factor: interaction with angiotensin II and adrenocorticotropin during variations of dietary sodium.

We investigated the in vitro steroidogenic activity of a new aldosterone-stimulating factor (ASF). Aldosterone responses of adrenal zona glomerulosa cells to ASF were assessed in response to variations in sodium intake and during incubation with either ACTH or angiotensin II (AII). Studies were performed in collagenase-dispersed adrenal capsular cells harvested from male New Zealand White rabbits that were on either regular or low sodium diets for 7-10 days. ASF, AII, and ACTH produced dose-dependent increases in aldosterone production. In cells from sodium-replete rabbits, the concentrations required to elicit the half-maximum response (ED50) were 2.2 +/- 0.3 (+/-SE) X 10(-11), 7.2 +/- 1.1 X 10(-10), and 3.4 +/- 0.5 X 10(-8) M for ACTH, AII, and ASF, respectively. Sodium depletion increased maximal responses but not sensitivity to AII and ACTH; responses to ASF were essentially unchanged. Large concentrations of ASF (10(-7) M) potentiated AII-induced aldosterone responses of adrenal capsular cells from sodium-depleted, but not sodium-replete, rabbits. In marked contrast, similar concentrations of ASF inhibited ACTH-induced aldosterone production of adrenal capsular cells from both sodium-replete and sodium-depleted rabbits. It is concluded that ASF has its own intrinsic steroidogenic activity. Furthermore, although large concentrations of ASF potentiate AII responses in sodium-depleted animals, ASF inhibits the aldosterone-stimulating activity of ACTH in both sodium-replete and sodium-depleted animals.

Chemical renal medullectomy. Effect on urinary prostaglandin E2 and plasma renin in response to variations in sodium intake and in relation to blood pressure.

We have studied the possible vasodepressor role of the renal medulla by chemical medullectomy. Bromoethylamine hydrobromide (200 mg/kg) was injected to induce selective renal medullary necrosis in rats. The acute effects on sodium balance and long-term effects on blood pressure, plasma renin concentration (PRC) and urinary prostaglandin E2 (PGE2) were studied and compared with saline injected controls. There was an immediate and sustained increase in urine volume of low osmolality. Direct blood pressure in conscious free-moving animals was higher at 2 and 10 weeks after injection in medullary-damaged rats, although this was only significant at 10 weeks (136 +/- 3.3 vs 118 +/- 4.5 mm Hg, p less than 0.01). An initial negative sodium balance returned to normal by 7 days and rats with established medullary damage tolerated a wide range of sodium intakes. Although there was no evidence of sodium retention on the normal diet, with very high sodium loads some sodium retention was apparent since PRC was suppressed and body weight increased. Plasma creatinine and creatinine clearance were normal. PRC in rats with medullary damage was unchanged on normal diet and rose to similar levels as in control rats on low sodium intake. Urinary PGE2 was markedly reduced (148 +/- 54 vs 536 +/- 71 ng/day, p less than 0.01) in medullary damaged rats, consistent with the renal medulla being the major source of urinary PGE2. High salt intake increased urinary PGE2 in normal and proportionally in medullary damaged rats, whereas on a low sodium intake, urinary PGE2 was not different from that on the normal diet in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac malformations in the fetal alcohol syndrome

ingesting a high-sodium diet was caused by inadequate sodium repletion. Two of our patients had high serum desoxycorticosterone and corticosterone concentrations and high urinary free desoxycorticosterone, free 18-hydroxYdesoxyc0rticosterone; and 18-hydroxYcorticoster0ne excretion in addition to the hyperaldosteronism. Variation in sodium intake resulted in changes in serum and urinary concentrations of these hormones, pa(allel to the changes in PRA and aldosterone. The high levels of desoxycorticosterone and corticosterone and their metabolites were most likely not the result of ACTH stimulation, since serum cortisol and urinary 17-hydroxysteroid values were not concomitantly elevated. Rather, as has been postulated, the renin-angiotensin SYstem may have directly stimulated these mineralocorticoids. ~ Normal to slightly elevated urinary aldosterone excretion 8 and plasma aldosterone and aldosterone secretion rates 9 have been reported in older, nonstressed children with CF. Simopoulous et al 1~ reported findings similar to ours in five - ~- .... :,t. ,~ ~A ~z~'/- to ...... vauc~lt~ warn ~.~l a~ct~ z., ycm~. Our findings confirm that excessive loss of electrolytes in the sweat of patients with CF, at times aggravated by vomiting, may lead to a state of intravascular volume contraction with resultant hyperreninemia and hyperaldosteronism. The finding of selective enlargement of the zona glomerulosa in the adrenals of young children with CF 11 suggests that volume depletion may indeed be chronic and have gone undetected.