Effect of Water Restriction during Adaptation to a Low-Sodium Diet in Man

1995 ◽  
Vol 89 (3) ◽  
pp. 305-310
Author(s):  
M. Sutters ◽  
W. S. Peart

1. Plasma sodium concentration may influence renal sodium excretion. We have examined the possibility that the fall in plasma sodium that occurs during salt restriction in man might be an important stimulus for renal sodium conservation. 2. In order to prevent the fall in plasma sodium that usually occurs during dietary salt restriction, we water restricted (200 ml/day) six normal subjects for the 2 days after the transition from 260 (high-sodium diet, day 3) to 20 mmol (low-sodium diet, days 4 and 5) sodium per day. In the control (hydrated) group water intake was held constant at 1800 ml/day. 3. Plasma sodium fell during the low-sodium diet in the hydrated group but remained constant in the dehydrated group (141.3 ± 0.2 to 140.2 ± 0.2 mmol/l versus 141.1 ± 0.3 to 141.3 ± 0.3 mmol/l). Plasma arginine vasopressin concentration was significantly higher and urine flow lower during the low-sodium diet in the dehydrated group (arginine vasopressin on day 5: hydrated group, 0.72 ± 0.1 pmol/l; dehydrated group, 2.18 ± 0.5 pmol/l). Weight fell by a similar amount in both groups (hydrated group, 1.23 ± 0.17 kg; dehydrated group, 1.45 ± 0.19 kg). 4. On the low-sodium diet there were no differences between groups in changes in plasma renin activity (hydrated group, 1.6 ± 0.24 to 4.78 ± 0.65 nmol angiotensin I h−1 ml−1; dehydrated group 1.57 ± 0.18 to 5.14 ± 0.56 nmol angiotensin I h−1 ml−1) or atrial natriuretic peptide (hydrated group, 23 ± 2.3 to 14.7 ± 1.6 pg/ml; dehydrated group, 26.8 ± 3.6 to 12.7 ± 1.3 pg/ml). Salivary aldosterone concentration increased further in the dehydrated study, but only on day 5. 5. Sodium excretion fell further in the dehydrated group over the first 16 h of the low-sodium diet on day 4 (hydrated group, 8.62 ± 0.76 mmol/h; dehydrated group, 6.57 ± 0.38 mmol/h). Creatinine clearance fell on day 5 (low sodium) in the dehydrated group but did not change significantly in the hydrated group (hydrated group, 152 ± 7 to 137 ± 7; dehydrated group, 157 ± 7 to 123 ± 7 ml/min). 6. We conclude that the fall in plasma sodium during salt restriction is not an important trigger for renal sodium conservation in man. The principal difference between studies was the elevation of arginine vasopressin in the dehydrated study. Differences in salivary aldosterone concentration occurred on day 5 only, too late to account for the differences in sodium excretion on day 4. Under the conditions of this study, our findings could be explained if physiological range elevation of arginine vasopressin has an antinatriuretic effect.

1993 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
M. Sutters ◽  
D. J. S. Carmichael ◽  
S. L. Lightman ◽  
W. S. Peart

1. A diuresis occurs within the first 36 h of salt restriction. A decline in plasma arginine vasopressin concentration may contribute to both the diuresis and antinatriuresis. 2. We have studied six normal human subjects during 36 h of dietary sodium restriction. In one study subjects received an intravenous infusion of D-glucose, and in the other an infusion of arginine vasopressin (6 fmol min−1 kg−1). 3. In the D-glucose phase plasma arginine vasopressin concentration fell (1.77 +034 to 1.02 +0.13 pg/ml), urine flow increased (67.9 +113 to 89.8 + 17.1 ml/h), haemoconcentration occurred (packed cell volume 40.8 +0.3 to 42.8 +03%, protein concentration 71.6 +03 to 74.5 + 0.6 g/l), plasma sodium concentration fell (140 +0.2 to 138 +0.2 mmol/l) and plasma renin activity increased (1600+153 to 3700 + 356 pg of angiotensin I h−1 ml−1). 4. In the arginine vasopressin phase plasma arginine vasopressin concentration remained constant (13 + 0.13 to 134 +0.11 pg/ml), the diuresis was reversed (65.7 +9.9 to 52.1 +8.9 ml/h), plasma sodium concentration fell further (139.8 +0.4 to 136.1 +0.4 mmol/l), the rise in plasma renin activity was reduced (arginine vasopressin 2552 + 292; D-glucose, 3700 + 356 pg of angiotensin I h−1 ml−1) and creatinine clearance was lower in the last 12 h of salt restriction (arginine vasopressin, 96.1 +6.9; D-glucose 116.5 + 6.8 ml/min). Renal sodium excretion was unaffected by arginine vasopressin infusion. 5. We conclude that the fall in plasma arginine vasopressin concentration during dietary salt restriction, whilst not affecting renal sodium excretion, may be important in the regulation of plasma sodium concentration, plasma renin activity and glomerular filtration.


1957 ◽  
Vol 189 (1) ◽  
pp. 181-184 ◽  
Author(s):  
M. Jay Goodkind ◽  
Wilmot C. Ball ◽  
James O. Davis

Chronic hemorrhage in normal dogs resulted in increased urinary aldosterone-like activity and a reduction in renal sodium excretion which was approximately equivalent to the sodium content of the blood removed. Glomerular filtration rate either increased or did not change. A comparable increase in aldosterone-like activity was observed in urine from normal dogs fed a low sodium diet equivalent to the net sodium intake of dogs subjected to hemorrhage.


1978 ◽  
Vol 58 (4) ◽  
pp. 597-604
Author(s):  
C. Y. PANG ◽  
L. D. CAMPBELL ◽  
G. D. PHILLIPS

Significantly lower feed intake, higher water intake and depressed growth rate were observed in poults under 30 days of age offered ad libitum a low (0.05%) sodium diet and tap water compared to control poults offered the same basal diet containing 0.25% added sodium. Mortality with dehydration occurred mainly between 2 and 3 wk of age in poults fed the low sodium diet. Significant pathophysiological changes in poults fed low sodium diet compared with the control on days 9–30 were: lower plasma sodium, chloride and osmolal concentrations; higher plasma contents of uric acid and total protein; higher packed cell volume; and lower body sodium and water contents. Indications of extracellular dehydration and intracellular hydration and decreased glomerular filtration rate in sodium-deficient poults are discussed. Plasma and body composition of poults fed the low sodium diet returned to normal 1 wk after the poults were offered a normal (0.25%) sodium diet and tap water ad libitum.


1980 ◽  
Vol 94 (3) ◽  
pp. 381-388 ◽  
Author(s):  
Eva Tarján ◽  
András Spät ◽  
Tamás Balla ◽  
Annamária Székely

Abstract. The purpose of the present study was to evaluate the role of the renin-angiotensin system in the secretion of aldosterone during restriction of dietary sodium intake. Rats were kept on control or low-sodium diet for one week. On the 7th morning of diet osmotic minipumps filled with the angiotensin converting enzyme inhibitor (CEI) SQ 20,881, or empty pumps, were implanted subcutaneously (sc). The rats were sacrificed 23 h later. Peripheral blood was analyzed for hormones and electrolytes. Adrenal capsular tissue (z. glomerulosa) was incubated for the determination of the conversion of [3H]corticosterone to [3H]aldosterone. Sodium depletion had no effect on plasma sodium, but it increased potassium concentration. Infusion of CEI had no significant effect on plasma electrolytes. Plasma renin activity was increased both by sodium depletion and CEI. The mean serum aldosterone level was twelve times higher in sodium depleted animals than in controls. Aldosterone level was reduced by about 60 per cent in CEI-infused animals both on control and low-sodium diet. The conversion of corticosterone to aldosterone was significantly stimulated by sodium deprivation. This effect was also inhibited by the CEI SQ 20,881.


1996 ◽  
Vol 270 (3) ◽  
pp. F406-F410
Author(s):  
K. A. Duggan ◽  
V. Z. Ye ◽  
D. M. Jones ◽  
G. J. Macdonald

Natriuresis in direct response to a gastric sodium stimulus (upper-gut sodium monitor) has paradoxically only been demonstrated in humans and animals on a low-sodium diet preceding each study. It is possible that the low-sodium diet itself induces or suppresses systems that mediate or oppose the ensuing natriuresis. In this study, we sought to determine whether a system activated by this diet, the renin-angiotensin system, mediates the natriuretic response. Specifically, we sought to show whether changes in the circulating concentration of angiotensin II (ANG II) may mediate the renal response to stimulation of the gastric sodium monitor. Male New Zealand White rabbits were randomly assigned to low- (0.008%) or normal (2.2%) sodium diets. After 1 wk on the experimental diet, they received a sodium load intragastrically or intravenously, and plasma ANG II was measured at 0, 5, 10, 30, 60, and 120 min. Urine was collected for 4 h after the sodium load, and plasma sodium was measured at 0, 2, and 4 h. Urinary sodium excretion was greater in the 4 h after gastric than after intravenous sodium administration (P < 0.025) in the rabbits on the low-sodium diet. No significant difference was noted in the rabbits on the normal sodium. In rabbits on the low-sodium diet, there was an immediate and significant decline in plasma ANG II after sodium was administered both intragastrically (P < 0.025) and intravenously (P < 0.05). This decrease was greater after intragastric than intravenous sodium (P < 0.0025), and the difference was still evident at 120 min (P < 0.05). No significant difference in plasma ANG II was found in the normal diet group. We conclude, therefore, that a prolonged decrease in ANG II concentration may play a role in mediating the natriuretic response to the gastric sodium monitor.


1976 ◽  
Vol 230 (6) ◽  
pp. 1504-1508 ◽  
Author(s):  
RM Carey ◽  
Smith ◽  
EM Ortt

Recent studies of sodium-depleted rabbits have shown that oral sodium loading is followed by greater natriuresis than intravenous sodium loading. The present study was undertaken to determine if this is dependent on differences in aldosterone excretion. Rabbits in balance on a low-sodium diet were given bolus doses of sodium either orally or intravenously. Those receiving oral sodium responded with a greater natriuresis than those receiving it intravenously. No differences in aldosterone excretion were demonstrated after oral or intravenous sodium repletion. Rabbits given large doses of exogenous aldosterone continued to excrete more sodium after oral than after intravenous repletion. This study demonstrates that in rabbits the gastrointestinal tract functions to regulate renal sodium excretion and that the mechanism is independent of aldosterone.


1979 ◽  
Vol 56 (3) ◽  
pp. 261-264 ◽  
Author(s):  
N. S. Oates ◽  
S. G. Ball ◽  
C. M. Perkins ◽  
M. R. Lee

1. Plasma and urine free dopamine were measured daily for 5 days in six normal subjects maintained on a low sodium diet. The subjects were then given dietary supplements of sodium chloride for 5 days and the measurements repeated. 2. Throughout the experiment the 24 h free dopamine excretion rates for all the subjects were higher than could be accounted for by renal clearance. Dopamine excretion increased significantly in response to the added sodium chloride whereas plasma dopamine remained unchanged. The rise in dopamine excretion preceded that of sodium excretion. 3. It is concluded that free dopamine is formed within the kidney in response to increased dietary sodium and may have a role in the control of sodium excretion.


Sign in / Sign up

Export Citation Format

Share Document