HYPERALDOSTERONISM IN THE SODIUM-DEPLETED RAT: MECHANISM OF ALDOSTERONE STIMULATION BY PERITONEAL DIALYSIS WITH GLUCOSE SOLUTION

1979 ◽  
Vol 82 (1) ◽  
pp. 17-25 ◽  
Author(s):  
A. SPÄT ◽  
K. NAGY ◽  
TARJÁN ÉVA

SUMMARY Peritoneal dialysis with 5% glucose solution was carried out in dexamethasone-pretreated rats. Dialysis brought about a severe loss of sodium and a slight loss of potassium into the peritoneal fluid. This kind of sodium depletion took place without any decrease in total body-water space, thus it evoked a severe fall in plasma sodium concentration. Plasma renin activity and the serum concentration of aldosterone increased in response to dialysis. Peak values in renin activity were attained within 60 min, whereas aldosterone concentrations exhibited a continuous rise until at least 120 min. Despite the correlation of renin and aldosterone values, neither the administration of an angiotensin I converting enzyme inhibitor (SQ 20,881) nor the reduction of plasma renin activity by indomethacin could reduce hyperaldosteronism evoked by peritoneal dialysis. Therefore, it is assumed that there is no causal relationship between renin and aldosterone in this kind of acute, severe sodium depletion.

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.


1981 ◽  
Vol 89 (3) ◽  
pp. 411-416 ◽  
Author(s):  
T. BALLA ◽  
K. NAGY ◽  
ÉVA TARJÁN ◽  
G. RENCZES ◽  
A. SPÄT

The present experiments were designed to study the effect of extracellular hyponatraemia on aldosterone secretion. Hyperaldosteronism was induced by peritoneal dialysis with 5% glucose solution in dexamethasone-pretreated rats. In the narrow physiological range of 135–142 mmol/l, as well as in the whole range of the study (122–142 mmol/l), the plasma concentration of sodium showed a close negative correlation with the serum concentration of aldosterone (r = −0·71 and −0·83, respectively). Plasma renin activity increased after peritoneal dialysis; however, no close correlation was observed either between sodium concentration and plasma renin activity or plasma renin activity and serum aldosterone concentration within the dialysed group. The ratio of serum concentration of aldosterone to plasma renin activity showed no considerable change between 132 and 142 mmol/l but rose steeply below 132 mmol sodium/l suggesting that a factor(s) other than angiotensin may also contribute to the induction of hyperaldosteronism.


1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.


1983 ◽  
Vol 244 (2) ◽  
pp. R244-R248 ◽  
Author(s):  
C. C. Barney ◽  
R. M. Threatte ◽  
M. J. Fregly

The role of angiotensin II in the control of water intake following deprivation of water for varying lengths of time was studied. Male rats were deprived of water for 0, 12, 24, 36, or 48 h. Water intakes were measured with and without pretreatment with the angiotensin I-converting enzyme inhibitor, captopril (50 mg/kg, ip). Captopril had no significant effect on water intake following either 0 or 12 h of water deprivation. However, captopril significantly attenuated water intake following 24-48 h of water deprivation with the magnitude of the attenuation increasing as the length of the period of water deprivation increased. Plasma renin activity was significantly increased over control levels after 24-48 h of water deprivation but not after 12 h of water deprivation. Plasma renin activity tended to increase as the length of the water-deprivation period increased. Serum osmolality and sodium concentration were significantly increased over control levels following 12-48 h of water deprivation. Serum osmolality and sodium concentration failed to show any further increases with increasing length of water deprivation beyond the increases following 12 h of water deprivation. The data indicate that the water intake of water-deprived rats can be divided into an angiotensin II-dependent component and angiotensin II-independent component. The angiotensin II-independent component appears to be more important in the early stages of water deprivation whereas the angiotensin II-dependent component becomes more important as the length of the water-deprivation period increases.


1978 ◽  
Vol 44 (6) ◽  
pp. 926-930 ◽  
Author(s):  
J. P. Finberg ◽  
R. Yagil ◽  
G. M. Berlyne

Plasma renin activity (PRA), renin substrate concentration (PRS), aldosterone concentration (PA), and cortisol levels were determined in five camels during dehydration (8–10 days complete denial of water) and at timed intervals after rapid rehydration in cool spring and hot summer weather. Plasma sodium concentration increased from 138 +/- 3.7 to 147 +/- 2.5 (mean +/- SE) meq/l during spring dehydration, and from 146 +/- 1.3 to 157 +/- 1.14 meq/l during dehydration in the summer. Plasma sodium concentration returned to control levels over the course of several hours following rapid rehydration. Only minor changes in plasma potassium concentration occurred. The hormonal changes were accentuated in the summer dehydration. PRA increased slightly on dehydration, and returned to control levels over the course of several hours following rehydration. PA increased slightly on dehydration but was markedly elevated 24 h after rehydration. PRS showed a slight increase following rehydration in the spring experiment, but no significant change in the summer experiment. Changes in cortisol were insignificant. The results are consistent with a role for angiotensin and aldosterone in enhancing sodium and water reabsorption from kidney and large intestine on dehydration in this species.


2005 ◽  
Vol 288 (6) ◽  
pp. F1113-F1117 ◽  
Author(s):  
Minhtri K. Nguyen ◽  
Ira Kurtz

Alterations in the plasma water sodium concentration ([Na+]pw) result from changes in the total exchangeable sodium (Nae), total exchangeable potassium (Ke), and total body water (TBW). The empirical relationship between the [Na+]pw and Nae, Ke, and TBW was originally demonstrated (Edelman IS, Leibman J, O'Meara MP, and Birkenfeld LW. J Clin Invest 37: 1236–1256, 1958), where [Na+]pw = 1.11(Nae + Ke)/TBW − 25.6 ( Eq. 1 ). Based on Eq. 1 , alterations in the [Na+]pw can be predicted by considering changes in the mass balance of Na+, K+, and H2O. In accounting for the mass balance of Na+, K+, and H2O in patients on peritoneal dialysis, considerations must also be taken to determine the modulating effect of dialysate clearance of Na+ and K+ and fluid changes resulting from this therapeutic modality on the [Na+]pw. In this article, we derive a new formula for predicting alterations in the plasma Na+ concentration ([Na+]p) in patients on peritoneal dialysis, taking into consideration the empirical relationship between the [Na+]pw and Nae, Ke, and TBW ( Eq. 1 ) as well as changes in mass balance of Na+ + K+ and H2O.


1980 ◽  
Vol 59 (s6) ◽  
pp. 101s-103s ◽  
Author(s):  
J. R. Sowers ◽  
M. L. Tuck ◽  
J. Barrett ◽  
M. P. Sambhi ◽  
M. S. Golub

1. In rats, intra-arterial metoclopramide, a dopamine antagonist, resulted in an elevation of plasma aldosterone at 5 min and plasma renin activity at 10 min and peak aldosterone and renin responses at 10 and 30 min respectively. 2. Pre-administration of l-dopa blunted and delayed aldosterone and renin responses to metoclopramide, indicating that metoclopramide-induced plasma aldosterone and plasma renin activity increments are mediated by a direct effect of blockade of dopamine receptors rather than other effects of this drug. 3. Pre-administration of angiotensin converting enzyme inhibitor, captopril (SQ 14 225) and the angiotensin II antagonist, saralasin, as well as bilateral nephrectomy did not significantly affect the aldosterone response to metoclopramide, Thus dopaminergic modulation of aldosterone secretion occurs independently of alterations in the renin-angiotensin system. 4. Modulating effects of dopamine on plasma aldosterone are probably mediated by direct effects as well as by interaction with other factors influencing aldosterone secretion at the adrenal zona glomerulosa.


1976 ◽  
Vol 51 (s3) ◽  
pp. 551s-554s
Author(s):  
H. M. Brecht ◽  
E. Werner ◽  
W. Schoeppe

1. The effect of long-term treatment with prindolol on blood pressure, total body potassium (Kt), exchangeable sodium (Nae) and plasma renin activity was investigated in twelve patients with essential hypertension. 2. Systolic and diastolic pressures were significantly reduced from 164/112 to 127/90 mmHg under basal conditions. 3. Before treatment Na. in patients with essential hypertension was significantly higher than in normotensive individuals. After an average of 16 weeks on prindolol Nae in patients with essential hypertension was significantly decreased, despite an average increase in body weight of 2 kg in the patients. 4. In contrast to the decrease in Nae, Kt was found to be significantly increased after long-term treatment with prindolol. Kt values of patients before and after prindolol, however, did not differ significantly from the corresponding sex- and age-dependent normal values. 5. Plasma renin activity was slightly diminished under basal and orthostatic conditions; the stimulatory effect of orthostasis was not abolished but reduced by prindolol. 6. It is suggested that the changes in sodium balance contribute to the anti-hypertensive effect of prindolol in patients with essential hypertension.


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