Effect of a Low Sodium Diet on Aldosterone-Stimulating Activity Of Angiotensin II in Dogs

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.

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1999.276.2.e303 ◽

1999 ◽

Vol 276 (2) ◽

pp. E303-E309 ◽

Cited By ~ 8

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.

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

Clinical Science ◽

10.1042/cs0500285 ◽

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.

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

Journal of Hypertension ◽

10.1097/00004872-200412000-00018 ◽

2004 ◽

Vol 22 (12) ◽

pp. 2355-2361 ◽

Cited By ~ 24

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

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

Acta Endocrinologica ◽

10.1530/acta.0.0960361 ◽

1981 ◽

Vol 96 (3) ◽

pp. 361-369 ◽

Cited By ~ 3

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.

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Angiotensin II: a humoral mediator for the gastric sodium monitor

AJP Renal Physiology ◽

10.1152/ajprenal.1996.270.3.f406 ◽

1996 ◽

Vol 270 (3) ◽

pp. F406-F410

Author(s):

K. A. Duggan ◽

V. Z. Ye ◽

D. M. Jones ◽

G. J. Macdonald

Keyword(s):

Angiotensin Ii ◽

Diet Group ◽

Plasma Sodium ◽

Ang Ii ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Significant Difference ◽

Sodium Load ◽

Intravenous Sodium

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.

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Oxytocin response to controlled dietary sodium and angiotensin II among healthy individuals

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00190.2018 ◽

2018 ◽

Vol 315 (4) ◽

pp. E671-E675 ◽

Cited By ~ 1

Author(s):

Suman Srinivasa ◽

Anna Aulinas ◽

Timothy O’Malley ◽

Patrick Maehler ◽

Gail K. Adler ◽

...

Keyword(s):

Angiotensin Ii ◽

Sodium Intake ◽

Dietary Sodium ◽

Ang Ii ◽

Healthy Individuals ◽

Fasting Serum ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Before And After

Oxytocin, while classically known for its role in parturition, lactation, and social behavior, also has been implicated in the control of sodium homeostasis in animal models. To improve our understanding of oxytocin physiology in humans, we measured basal oxytocin levels under low- and liberal-dietary-sodium conditions and following a peripheral angiotensin II (ANG II) infusion. Ten healthy individuals underwent a 6-day standardized low-sodium diet and a 6-day liberal-sodium diet. Each diet was followed by a graded ANG II infusion for 30-min sequential intervals at doses of 0.3, 1.0, and 3.0 ng·kg−1·min−1. Fasting serum oxytocin was assessed before and after ANG II infusion. Basal oxytocin levels (1,498.5 ± 94.7 vs. 1,663.3 ± 213.9 pg/ml, P = 0.51) did not differ after the low- and liberal-sodium diets. Following the ANG II infusion, ANG II levels and mean arterial pressure significantly increased as expected. In contrast, the ANG II infusion significantly lowered oxytocin levels from 1,498.5 ± 94.7 vs. 1,151.7 ± 118.1 pg/ml ( P < 0.001) on the low-sodium diet and from 1,663.3 ± 213.9 vs. 1,095.2 ± 87.4 pg/ml ( P = 0.03) on the liberal-sodium diet. The percent change in oxytocin following the ANG II infusion did not differ by sodium diet (−25 ± 5% vs. −28 ± 7% low- vs. liberal-sodium conditions, P > 0.99). Dietary sodium intake did not affect circulating oxytocin levels among healthy individuals. Systemic oxytocin levels were significantly suppressed following a peripheral ANG II infusion independent of dietary sodium conditions.

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Angiotensin augments epinephrine release in pithed rats fed a low-sodium diet

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.258.1.r187 ◽

1990 ◽

Vol 258 (1) ◽

pp. R187-R192 ◽

Cited By ~ 1

Author(s):

R. R. Vollmer ◽

S. P. Corey ◽

S. A. Meyers ◽

E. M. Stricker ◽

S. J. Fluharty

Keyword(s):

Angiotensin Ii ◽

Sodium Intake ◽

Renin Angiotensin System ◽

Dietary Sodium ◽

Angiotensin System ◽

Renin Angiotensin ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Pithed Rats

In confirmation of previous studies, the amount of epinephrine released into blood during electrical stimulation of the thoracolumbar region of the spinal cord in pithed rats on a low-sodium diet (0.01% sodium by weight of diet for 1 mo) was significantly greater than that observed in rats on a normal sodium diet (0.3% sodium by weight of diet). The present work assessed the extent to which endogenously formed angiotensin II influences this neurally mediated adrenal epinephrine release. The augmented release of epinephrine in rats maintained on the low-sodium diet appeared to depend on circulating angiotensin II because blockade of angiotensin II receptors with saralasin decreased the epinephrine release in these animals but not in rats maintained on the normal diet. Similar results were obtained when the renin-angiotensin system was blocked with the converting-enzyme inhibitor captopril. Adrenal epinephrine content was not affected by the dietary sodium intake; however, the catecholamine synthetic capacity was augmented as indicated by a significant induction of tyrosine hydroxylase. In addition, the adrenal medullary angiotensin II receptor density was significantly elevated in animals on the low-sodium diet. These results demonstrate that endogenous angiotensin II is capable of providing a positive modulatory influence on neurally mediated release of adrenal epinephrine, an effect that may require a chronic activation of the renin-angiotensin system as occurs naturally with restricted dietary sodium intake.

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Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake

Reproduction ◽

10.1530/rep.1.00565 ◽

2006 ◽

Vol 131 (2) ◽

pp. 331-339 ◽

Cited By ~ 13

Author(s):

Jean St-Louis ◽

Benoît Sicotte ◽

Annie Beauséjour ◽

Michèle Brochu

Keyword(s):

Angiotensin Ii ◽

Salt Intake ◽

Sodium Intake ◽

High Salt ◽

Pregnant Rats ◽

High Sodium ◽

Sodium Diet ◽

Uterine Arteries ◽

Low Sodium Diet ◽

Low Sodium

Lowering and increasing sodium intake in pregnant rats evoke opposite changes in renin–angiotensin–aldosterone system (RAAS) activity and are associated with alterations of blood volume expansion. As augmented uterine blood flow during gestation is linked to increased circulatory volume, we wanted to determine if low- and high-sodium intakes affect the mechanical properties and angiotensin II (AngII) responses of the uterine vasculature. Non-pregnant and pregnant rats received a normal sodium (0.22% Na+) diet. On the 15th day of gestation some animals were moved to a low-sodium (0.03%) diet, whereas others were given NaCl supplementation as beverage (saline, 0.9% or 1.8%) for 7 days. All rats were killed after 7 days of treatment (eve of parturition). Uterine arcuate arteries (>100 μm) were set up in wire myographs under a tension equivalent to 50 mmHg transmural pressure. The pregnancy-associated increase in diameter of the uterine arteries was significantly attenuated on the low-sodium diet and 1.8% NaCl supplementation. The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium supplementation of non-pregnant rats did not affect the reactivity of the uterine arteries to AngII, but significantly reduced the effect of Phe (1 μmol/l). High salt also significantly diminished the elevated responses to AngII in the arteries of pregnant animals. It was observed that altered sodium intake affects the mechanical and reactive properties of the uterine arcuate arteries more importantly in pregnant than in non-pregnant rats. Low-salt intake similarly affected the reactivity of the uterine arcuate arteries to AngII and Phe, whereas high-salt intake more specifically affected AngII responses. These results showed that perturbations of sodium intake have major impacts on the structure and functions of the uterine arterial circulation, indicating RAAS involvement in uterine vascular remodeling and function during gestation.

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Evidence that the Acute Cardiovascular Response to Isoprenaline is Partly Mediated via Renin Release

Clinical Science ◽

10.1042/cs0570013 ◽

1979 ◽

Vol 57 (1) ◽

pp. 13-18 ◽

Cited By ~ 1

Author(s):

G. H. Anderson

Keyword(s):

Angiotensin Ii ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Plasma Renin Activity ◽

Infusion Rate ◽

Plasma Renin ◽

Renin Activity ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium

1. The possible effect of the increased plasma renin activity induced by β−adrenoreceptor stimulation in supporting arterial pressure has been studied in five normal subjects on a diet of 100 mmol of sodium/day for 4 days or 40 mmol of sodium/day for 4 days by infusing isoprenaline at 1·0, 2·0 or 3·0 μg min−170 kg−1, each for 1 h with 45 min between each infusion rate. During the last 30 min of each isoprenaline dose, the angiotensin II analogue [Sar1, Ala8]angiotensin II (saralasin) was infused. 2. Isoprenaline significantly (at least P <0·05) increased the pulse rate, systolic arterial pressure and plasma renin activity; the diastolic blood pressure decreased but the mean arterial pressure did not change. Saralasin administered to subjects on the 100 mmol of sodium/day diet significantly (at least P < 0·05) lowered mean arterial pressure at the two highest isoprenaline infusion rates. 3. With patients on a low sodium diet, saralasin lowered mean arterial pressure at all three isoprenaline infusion rates. On the low sodium diet the fall in mean arterial pressure caused by saralasin was significantly greater (P < 0·05) at the isoprenaline infusion rate of 3·0 μg min−1 70 kg−1 than at the infusion rate of 1·0 μg min−1 70 kg−1. The change in mean arterial pressure with saralasin before and during isoprenaline infusion on both diets was significantly correlated (r = −0·39, n = 38, P < 0·01) with the plasma renin activity measured immediately before saralasin infusion. 4. It is concluded that during β−adrenoreceptor stimulation the increased plasma renin activity (acting through angiotensin) supports arterial pressure.

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