Aldosterone response to sodium deprivation and angiotensin II in patients with hypopituitarism

1981 ◽  
Vol 96 (3) ◽  
pp. 361-369 ◽  
Author(s):  
Cornelia Seifert ◽  
Wolfgang Oelkers
Keyword(s):  
Angiotensin Ii ◽  
Pituitary Gland ◽  
Blood Pressure Response ◽  
Normal Subjects ◽  
Zona Glomerulosa ◽  
Sodium Balance ◽  
Sodium Deficiency ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract. Unknown pituitary factor(s) apart from ACTH may participate in the regulation of aldosterone (aldo) secretion in man. We investigated whether the 'sensitization' of the zona glomerulosa against angiotensin II (A II) by sodium deficiency was mediated by the pituitary gland. A II was infused in stepwise increasing doses (2, 4, 8 ng/kg/min) into 5 normal subjects (N) and into 8 patients with hypopituitarism (H) before and after 4 days on a low sodium diet. Mean cumulative sodium balance after the low sodium diet was − 145 mm in N and − 165mm in H. Plasma-aldo and aldo-exretion rate on the normal sodium diet were slightly lower in H than in N but rose less than normal during sodium depletion in H. Plasma A II and renin activity on normal sodium were slightly higher in H than in N, but the increase on the low sodium diet was blunted in H. The stimulation of plasmaaldo by A II infusion was similar in both groups on the normal sodium diet. In both groups, the response of P-aldo to A II infusion was greater in the sodium deplete than in the replete state, although 'sensitization' was slightly less marked in H than in N. This may be due to the blunted rise of plasma-A II after sodium loss in H, which may also account for abnormalities in the blood pressure response in the H group. Altogether, the results speak against a direct involvement of the pituitary gland in 'sensitization', but an indirect influence through unexplained abnormalities in renin secretion is possible.

Control of adrenal cell proliferation by AT1 receptors in response to angiotensin II and low-sodium diet

1999 ◽  
Vol 276 (2) ◽  
pp. E303-E309 ◽  
Author(s):  
Pauline E. McEwan ◽  
Gavin P. Vinson ◽  
Christopher J. Kenyon
Keyword(s):  
Cell Proliferation ◽  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Ang Ii ◽  
Adrenal Cell ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Glomerulosa Cells

The effects of angiotensin II (ANG II), the angiotensin type 1 (AT1) receptor antagonist losartan, and low-sodium diet on rat adrenal cell proliferation were studied in vivo with immunocytochemistry. Both ANG II and low-sodium diet increased proliferation of endothelial cells of the zona glomerulosa. Losartan prevented ANG II-induced hyperplasia of glomerulosa cells but not the effects of a low-sodium diet. Glomerulosa cells after ANG II + losartan treatment appeared hypertrophied compared with those of controls. Proliferative effects of ANG II and low-sodium diet in the reticularis were blocked by losartan. No changes were seen in the fasciculata. Proliferation in the medulla was increased with losartan, was decreased by ANG II, but was unaffected by low-sodium diet. In conclusion, 1) cell hypertrophy and proliferation of glomerulosa cells are mediated by AT1 receptor-dependent and -independent processes, 2) proliferation of reticularis cells is controlled by AT1 receptors, and 3) reciprocal control of chromaffin cell proliferation by ANG II may involve indirect AT1-dependent processes.

Hypotensive effect of [Sar1,Thr8]angiotensin II in spontaneously hypertensive sodium-depleted rats

1978 ◽  
Vol 234 (4) ◽  
pp. H447-H453
Author(s):  
H. Munoz-Ramirez ◽  
M. C. Khosla ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Normal Diet ◽  
Spontaneously Hypertensive ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Angiotensin Ii Antagonist

Under inactin anesthesia, intravenous infusion of [Sar1,Thr8]angiotensin II produced a hypotensive effect in young spontaneously hypertensive rats (SHR) treated with furosemide and in mature SH rats fed a low-sodium diet. The angiotensin antagonist also lowered blood pressure of young and mature SH rats receiving a normal diet. Deoxycorticosterone acetate (DOCA) plus saline reversed the hypotensive effect of [Saru,Thr8]angiotensin II in young SH rats, but did not do so in mature SH rats. Plasma renin activity (PRA) was not significantly changed by anesthesia. Furosemide or the low-sodium diet significantly increased PRA in young and mature SH rats. In contrast, DOCA plus saline significantly reduced PRA in both young and mature SH rats. However, there was no correlation between PRA and the action of the angiotensin II antagonist. These data suggest that the renin-angiotensin system is involved in genetic hypertension.

The Influence of Sodium Intake on the Pressor Response to Angiotensin II in the Unanaesthetized Rat

1976 ◽  
Vol 50 (4) ◽  
pp. 285-291
Author(s):  
Barbara L. Slack ◽  
J. M. Ledingham
Keyword(s):  
Angiotensin Ii ◽  
Dose Response ◽  
Response Curve ◽  
Dose Response Curve ◽  
Response Curves ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High Sodium Diet

1. Dose—response curves for the pressor activity of angiotensin II have been determined in unanaesthetized rats receiving diets containing 2·5% (w/w) or 0·007% (w/w) sodium; the different diets were administered in various sequences. 2. In comparison with those from rats receiving a low sodium diet, the dose—response curves were displaced to the left on the high sodium diet, indicating a greater response to angiotensin, and this displacement persisted for a period of approximately 7 days after the diet was changed from high to low sodium. The dose—response curve subsequently shifted to the right when the low sodium diet was maintained for longer. 3. There was a negative correlation between the slope of the dose—response curve and the basal blood pressure in all groups; the correlation was significant in three out of the five different treatment groups. 4. Basal blood pressures were significantly raised in rats on the high sodium diet for 7 days. 5. A number of possible mechanisms have been considered to explain both the parallel shift of the dose—response curve and alteration in its slope. It is concluded that the observed findings are compatible with an action of sodium-loading on the sensitivity of the smooth muscle cell to angiotensin, on the resting of the renin—angiotensin system, on the rate of in-activation of angiotensin and on a change in initial length of the muscle fibre.

EFFECT OF PROSTAGLANDIN SYNTHETASE INHIBITORS ON RENIN AND ALDOSTERONE IN MAN ON A NORMAL OR LOW SODIUM DIET

1978 ◽  
Vol 87 (3) ◽  
pp. 577-588 ◽  
Author(s):  
G. Norbiato ◽  
M. Bevilacqua ◽  
U. Raggi ◽  
P. Micossi ◽  
C. Moroni ◽  
...  
Keyword(s):  
Diclofenac Sodium ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Upright Position ◽  
Synthetase Activity ◽  
Prostaglandin Synthetase ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Before And After

ABSTRACT The effect of two inhibitors of prostaglandin synthetase activity (acetylsalicylic acid (ASA) and diclofenac sodium (DCFS)) on plasma renin activity (PRA) and plasma aldosterone (PA) was studied in normal subjects kept on a diet with constant sodium and potassium intake or on a low-salt diet for 7 days. In 9 subjects, 2 days of treatment with ASA (3 g/day) was followed by a significant decrease of PA in the supine position (after overnight rest); there was no significant decrease of PRA. However, both PA and PRA with the subjects in the upright position were significantly reduced after ASA. In 9 subjects treated with DCFS (200 mg for 2 days), both PA and PRA with the subjects in the supine and upright positions decreased significantly. Similar results were obtained from 4 subjects on a low-sodium diet (15–30 mEq./day) treated with DCFS (150 mg/day for 3 days). In contrast, no significant changes in PA or PRA with the subjects in the supine or upright position were observed in 4 subjects on a very low sodium diet (< 15 mEq./day) treated with DCFS (150 mg/day for 3 days). Covariance analysis (with PRA as independent variable and PA as dependent variable) of the data obtained in the upright position before and after treatment with ASA or DCFS showed that the decrease in PA remained significant after adjustment for the PRA effect. These results suggest a direct effect of prostaglandins on PA. The data obtained from subjects on a low sodium diet indicate that sodium deprivation may counteract the effects of DCFS on PRA and PA.

Renal nerves in renal adaptation to dietary sodium restriction

1983 ◽  
Vol 245 (3) ◽  
pp. F322-F328 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Renal Denervation ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Body Sodium ◽  
Renal Adaptation

To assess the physiologic importance of the renal nerves in the renal mechanisms for the maintenance of body sodium balance, renal adaptation to normal and low sodium diet was evaluated in conscious Sprague-Dawley male rats before and 8 days after recovery from bilateral surgical-pharmacological renal denervation. Renal denervation was confirmed in every rat at the end of the study by absence of renal vasoconstriction to splanchnic nerve stimulation and loss of renal tissue norepinephrine content. Daily sodium balance, defined as the difference between dietary sodium intake and urinary sodium excretion, was positive with the normal sodium diet before and after bilateral renal denervation. Prior to bilateral renal denervation, changing to the low sodium diet was associated with a diminishingly negative sodium balance for 3 days that became progressively positive thereafter. After bilateral renal denervation, changing to the low sodium diet was associated with a continuous and progressively negative sodium balance. We conclude that intact renal innervation is required for normal renal sodium conservation and maintenance of body sodium balance during dietary sodium restriction.

Low sodium diet inhibits the local counter-regulator effect of angiotensin-(1-7) on angiotensin II

2004 ◽  
Vol 22 (12) ◽  
pp. 2355-2361 ◽  
Author(s):  
Anton JM Roks ◽  
Jeroen Nijholt ◽  
Azuwerus van Buiten ◽  
Wiek H van Gilst ◽  
Dick de Zeeuw ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

scholarly journals Actions of vasoactive intestinal peptide on the rat adrenal zona glomerulosa

1999 ◽  
Vol 161 (1) ◽  
pp. 51-57 ◽  
Author(s):  
JP Hinson ◽  
S Kapas ◽  
Keyword(s):  
Binding Sites ◽  
Zona Glomerulosa ◽  
Control Group ◽  
Aldosterone Secretion ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Adrenergic Antagonist ◽  
Adrenergic Antagonists ◽  
Local Release

Previous studies, by this group and others, have shown that vasoactive intestinal peptide (VIP) stimulates aldosterone secretion, and that the actions of VIP on aldosterone secretion by the rat adrenal cortex are blocked by beta adrenergic antagonists, suggesting that VIP may act by the local release of catecholamines. The present studies were designed to test this hypothesis further, by measuring catecholamine release by adrenal capsular tissue in response to VIP stimulation. Using intact capsular tissue it was found that VIP caused a dose-dependent increase in aldosterone secretion, with a concomitant increase in both adrenaline and noradrenaline release. The effects of VIP on aldosterone secretion were inhibited by atenolol, a beta1 adrenergic antagonist, but not by ICI-118,551, a beta2 adrenergic antagonist. Binding studies were carried out to investigate VIP receptors. It was found that adrenal zona glomerulosa tissue from control rats contained specific VIP binding sites (Bmax 853+/-101 fmol/mg protein; Kd 2.26+/-0.45 nmol/l). VIP binding was not displaced by ACTH, angiotensin II or by either of the beta adrenergic antagonists. The response to VIP in adrenals obtained from rats fed a low sodium diet was also investigated. Previous studies have found that adrenals from animals on a low sodium diet exhibit increased responsiveness to VIP. Specific VIP binding sites were identified, although the concentration or affinity of binding sites in the low sodium group was not significantly different from the controls. In the low sodium group VIP was found to increase catecholamine release to the same extent as in the control group, however, in contrast to the control group, the adrenal response to VIP was not altered by adrenergic antagonists in the low sodium group. These data provide strong support for the hypothesis that VIP acts by the local release of catecholamines in adrenal zona glomerulosa tissue in normal animals. It does not appear that VIP acts through the same mechanism in animals maintained on a low sodium diet. The mechanism by which VIP stimulates aldosterone in this group remains to be determined.

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