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

1990 ◽  
Vol 258 (1) ◽  
pp. R187-R192 ◽  
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.

Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat

1980 ◽  
Vol 94 (3) ◽  
pp. 381-388 ◽  
Author(s):  
Eva Tarján ◽  
András Spät ◽  
Tamás Balla ◽  
Annamária Székely
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Sodium ◽  
Sodium Depletion ◽  
Angiotensin System ◽  
Aldosterone Level ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

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.

Aldosterone escape to chronic ACTH administration in man

1983 ◽  
Vol 103 (1) ◽  
pp. 116-124 ◽  
Author(s):  
Rolf C. Gaillard ◽  
Anne M. Riondel ◽  
Charles A. Favrod-Coune ◽  
Michel B. Vallotton ◽  
Alex F. Muller
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Aldosterone Secretion ◽  
Acth Stimulation ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Refractory State

Abstract. Prolonged ACTH administration produces a transient and self-limiting stimulation of aldosterone secretion which has been attributed to sodium retention, to inhibition of final enzymatic steps of aldosterone biosynthesis and/or to a morphological change of the glomerulosa cells. This study was undertaken to determine the possible role of the renin-angiotensin system in mediating the aldosterone escape to repeated ACTH stimulation. We studied in normal male volunteers the effect of a 4 day ACTH administration on urinary aldosterone metabolite excretion (3 oxo-conjugate and tetrahydroaldosterone) during concomitant diuretic administration (spironolactone or triamterene). In addition the plasma aldosterone response to acute iv stimulation with ACTH before and during the corticotrophin-induced 'refractory state' was examined both on normal and on low sodium diet. Spironolactone was unable to counteract the sodium retention induced by ACTH stimulation; aldosterone excretion showed the same transient increase as with ACTH alone while plasma renin activity remained low. Triamterene produced a negative sodium balance, a significantly more sustained increase in aldosterone excretion and an increase in plasma renin activity. In either situation the two metabolites of aldosterone showed the same pattern of excretion. The plasma aldosterone response to acute iv ACTH stimulation was completely blocked during the corticotrophin-induced 'refractory state' on normal sodium intake, whereas on low sodium diet a clear-cut response was still obtained. These data suggest that the transient effect of ACTH on aldosterone secretion is dependent on the state of activity of the renin-angiotensin system. When renin was stimulated by low sodium intake or sodium depletion, the aldosterone response to repeated ACTH administration was more sustained, and when renin was stimulated by low sodium intake, the aldosterone response to acute ACTH was maintained. In conclusion we suggest that the renin-angiotensin system is able to delay but not to suppress the changes induced in the zona glomerulosa by prolonged ACTH stimulation.

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

2018 ◽  
Vol 315 (4) ◽  
pp. E671-E675 ◽  
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.

Endothelial function during stimulation of renin-angiotensin system by low-sodium diet in humans

2001 ◽  
Vol 280 (5) ◽  
pp. H2248-H2254 ◽  
Author(s):  
Torbjørn Omland ◽  
Wendy Johnson ◽  
Mary Beth Gordon ◽  
Mark A. Creager
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Concomitant Treatment ◽  
Double Blind ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Stimulation Of

We examined whether physiological stimulation of the endogenous renin-angiotensin system results in impaired endothelium-dependent vasodilatation in forearm resistance vessels of healthy subjects and whether this impairment can be prevented by angiotensin II type 1 receptor blockade. A low-sodium diet was administered to 27 volunteers who were randomized to concomitant treatment with losartan (100 mg once daily) or matched placebo in a double-blind fashion. Forearm blood flow was assessed by venous occlusion plethysmography at baseline and after 5 days. Endothelium-dependent and -independent vasodilation was assessed by intra-arterial infusion of methacholine and verapamil, respectively. The low-sodium diet resulted in significantly decreased urine sodium excretion (placebo: 146 ± 64 vs. 10 ± 9 meq/24 h, P < 0.001; losartan: 141 ± 56 vs. 14 ± 14 meq/24 h, P < 0.001) and increased plasma renin activity (placebo: 1.0 ± 0.5 vs. 5.0 ± 2.5 ng · ml−1 · h−1, P < 0.001; losartan: 3.8 ± 7.2 vs. 19.1 ± 11.2 ng · ml−1 · h−1, P = 0.006) in both the losartan and placebo groups. With the baseline study as the reference, the diet intervention was not associated with any significant change in endothelium-dependent vasodilation to methacholine in either the placebo ( P = 0.74) or losartan ( P = 0.40) group. We conclude that short-term physiological stimulation of the renin-angiotensin system does not cause clinically significant endothelial dysfunction. Losartan did not influence endothelium-dependent vasodilation in humans with a stimulated renin-angiotensin system.

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.

Adrenergic control of renin during dietary sodium deprivation in conscious dogs

1989 ◽  
Vol 256 (6) ◽  
pp. E863-E871 ◽  
Author(s):  
H. Hisa ◽  
Y. H. Chen ◽  
K. J. Radke ◽  
J. L. Izzo ◽  
C. D. Sladek ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Conscious Dogs ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Adrenergic Stimulation ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Dietary Sodium Restriction

These experiments evaluated the contribution of alpha- and beta-adrenergic stimulation to plasma renin activity (PRA) during early and long-term dietary sodium restriction, compared with normal sodium intake. Uninephrectomized conscious dogs with catheters in the aorta, vena cava, and remaining renal artery were studied during normal sodium diet (approximately 70 meq/day), after 2-3 days of low-sodium diet (5-7 meq/day), and after greater than or equal to 2 wk of low-sodium diet. Direct renal arterial (ira) infusion of phenoxybenzamine plus propranolol decreased PRA by similar proportions (39-48%) during all three states of dietary sodium intake. The PRA achieved after adrenergic blockade remained higher (P less than 0.05) during early and long-term sodium restriction than during normal sodium intake. The effect on PRA of ira infusion of propranolol alone was not different from that of phenoxybenzamine plus propranolol during normal or low-sodium diet, and the magnitude of decrease in PRA during low-sodium diet was the same whether propranolol (1 microgram.kg-1.min-1) was infused ira or intravenously. In summary, beta-adrenergic stimulation accounts for similar proportions of PRA during early and long-term dietary sodium restriction and during normal sodium intake. Renal alpha-adrenoceptors appear to play little or no role in control of PRA under these conditions.

Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1–7) administration in anesthetized rats

2013 ◽  
Vol 304 (3) ◽  
pp. R260-R266 ◽  
Author(s):  
Julie O'Neill ◽  
Alan Corbett ◽  
Edward J. Johns
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renal Hemodynamic

Angiotensin II at the kidney regulates renal hemodynamic and excretory function, but the actions of an alternative metabolite, angiotensin (1–7), are less clear. This study investigated how manipulation of dietary sodium intake influenced the renal hemodynamic and excretory responses to intrarenal administration of angiotensin (1–7). Renal interstitial infusion of angiotensin (1–7) in anesthetized rats fed a normal salt intake had minimal effects on glomerular filtration rate but caused dose-related increases in urine flow and absolute and fractional sodium excretions ranging from 150 to 200%. In rats maintained for 2 wk on a low-sodium diet angiotensin (1–7) increased glomerular filtration rate by some 45%, but the diuretic and natriuretic responses were enhanced compared with those in rats on a normal sodium intake. By contrast, renal interstitial infusion of angiotensin (1–7) in rats maintained on a high-sodium intake had no effect on glomerular filtration rate, whereas the diuresis and natriuresis was markedly attenuated compared with those in rats fed either a normal or low-sodium diet. Plasma renin and angiotensin (1–7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. These findings demonstrate that the renal hemodynamic and excretory responses to locally administered angiotensin (1–7) is dependent on the level of sodium intake and indirectly on the degree of activation of the renin-angiotensin system. The exact way in which angiotensin (1–7) exerts its effects may be dependent on the prevailing levels of angiotensin II and its receptor expression.

Long-Term Adherence to Low-Sodium Diet in Patients With Heart Failure

2017 ◽  
Vol 39 (4) ◽  
pp. 553-567 ◽  
Author(s):  
Misook L. Chung ◽  
Linda Park ◽  
Susan K. Frazier ◽  
Terry A. Lennie
Keyword(s):  
Heart Failure ◽  
Patient Adherence ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Factors Affecting ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Positive Attitudes

Although following a low-sodium diet (LSD) for heart failure (HF) has been recommended for decades, little is known about factors related to long-term patient adherence. The purposes of this study were to (a) compare sodium intake and factors affecting adherence in a long-term adherent group and in a non-adherent group and (b) examine predictors of membership in the long-term adherent group. Patients with HF ( N = 74) collected 24-hr urine samples and completed the Dietary Sodium Restriction Questionnaire and the Patient Health Questionnaire-9. Long-term adherence was determined using the Stage of Dietary Behavior Change Scale. The long-term adherent group had lower sodium intake (3,086 mg vs. 4,135 mg, p = .01) and perceived more benefits from LSD than the non-adherent group. Only positive attitudes toward LSD predicted membership in the long-term adherence group (odds ratio [OR] = 1.18, p = .005). Interventions focused on enhancing positive perceptions of the benefits of an LSD may improve long-term dietary adherence in patients with HF.

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