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.

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.

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.

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.

Modulation of the intrahepatic renin–angiotensin system after stimulation of the gastric sodium monitor in the rat

1999 ◽  
Vol 98 (1) ◽  
pp. 57-64
Author(s):  
V. Z. C. YE ◽  
K. A. DUGGAN
Keyword(s):  
Renin Angiotensin System ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Sprague Dawley Rats ◽  
Sodium Load ◽  
Ace Activity ◽  
Stimulation Of

Changes in the rate of formation of angiotensin II (ANG II) participate in mediating the natriuresis that occurs in direct response to a gastric sodium stimulus (upper-gut sodium monitor). As this natriuresis is also dependent on intrahepatic events, we investigated whether changes in hepatic and plasma angiotensinogen levels and hepatic angiotensin-converting enzyme (ACE) activity might explain the decrease in ANG II synthesis. Male Sprague–Dawley rats, equilibrated on a low-sodium diet, were anaesthetized and received a sodium load of 1.5 mmol/kg (using 3× normal saline) either intragastrically or intravenously. Blood and livers were sampled before and at various times after sodium administration. ACE activity in serum and tissues was determined by generation of histidyl-leucine. Angiotensinogen was determined by radioimmunoassay of angiotensin I generated by incubation in the presence of exogenous renin. Plasma angiotensinogen had decreased significantly by 15 min after sodium administration (P< 0.005), while hepatic angiotensinogen was also decreased significantly from 30 min after the sodium load (P< 0.01). Hepatic ACE activity decreased in response to sodium (P< 0.005) from 30 min. We conclude that stimulation of the gastric sodium monitor regulates angiotensinogen synthesis and secretion by the liver, as well as hepatic ACE activity.

Myocardial renin is neither necessary nor sufficient to initiate or maintain ventricular hypertrophy

2000 ◽  
Vol 278 (3) ◽  
pp. R578-R586 ◽  
Author(s):  
Stephen A. Katz ◽  
John A. Opsahl ◽  
Shane E. Wernsing ◽  
Lynn M. Forbis ◽  
Juline Smith ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Salt Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Low Salt ◽  
Necessary And Sufficient

We tested the hypothesis that the myocardial renin-angiotensin system (RAS) is both necessary and sufficient to initiate and maintain all classes of ventricular hypertrophy. Myocardial and plasma renin and angiotensinogen were measured in rats during initiation and maintenance of ventricular hypertrophy associated with DOCA implants and 1% NaCl drinking water, with and without the AT1 ANG II receptor blocker losartan. Additional groups of rats were given a low-sodium diet (0.04%) for 3 wk. Ventricular hypertrophy was initiated within 7 days and maintained for 35 days in DOCA-treated rats despite significantly low myocardial and plasma renin, normal or low myocardial and plasma angiotensinogen, or the presence of losartan. Furthermore, there was no ventricular hypertrophy in low-salt diet-fed animals despite increased myocardial and plasma renin levels and normal angiotensinogen levels. Therefore, the myocardial RAS is not necessary to initiate or maintain cardiac hypertrophy in DOCA-treated rats and is not sufficient to initiate cardiac hypertrophy in low-salt diet-fed rats. Additionally, myocardial renin and angiotensinogen were significantly correlated with corresponding plasma levels.

The effect of chronic low-dose infusion of ACTH (1–24) on renin, renin-substrate, aldosterone and other corticosteroids in sodium replete and deplete man

1980 ◽  
Vol 95 (2) ◽  
pp. 198-206 ◽  
Author(s):  
Regina Fuchs-Hammoser ◽  
Martin Schweiger ◽  
Wolfgang Oelkers
Keyword(s):  
Plasma Levels ◽  
Low Dose ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Transient Effect ◽  
Aldosterone Secretion ◽  
Renin Substrate ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract. Low-dose infusions of ACTH 1-24 (5 U/day) of 4 days duration were performed in 2 healthy young men on a normal sodium diet and in 2 on a low sodium diet, in order to study the mechanism of the transient effect of ACTH on aldosterone secretion described by other authors using larger doses of ACTH. Cortisol secretion was continuously stimulated by ACTH. Plasma aldosterone (P-Al) and its urinary metabolites increased during the first two days of infusion and returned to control or below control levels subsequently. Plasma renin activity (PRA) was also transiently stimulated by ACTH. Changes in PRA were not caused by changes in plasma renin substrate concentration. The correlation between PRA and P-Al (r = + 0.78; n = 52) was highly significant (P < 0.01). Plasma levels of deoxycorticosterone (DOC), 18-OH-DOC and corticosterone were also transiently stimulated in subjects on a normal sodium diet, while the stimulation was better maintained in those on a low sodium diet. The results suggest that the transient effect of low-dose ACTH infusion on aldosterone secretion may in part be mediated by changes in the renin-angiotensin-system. Changes in plasma levels of angiotensin II, which controls early and late steps in the mineralocorticoid biosynthetic pathway, may determine the extent to which chronically elevated ATCH levels stimulate the release of aldosterone and, perhaps, even the release of DOC and corticosterone. On the normal sodium diet, sodium retention and a slight fall in serum potassium levels towards the end of ACTH infusion may have contributed to the depression of aldosterone release.

scholarly journals Transcription of (pro)renin mRNA in the rat adrenal cortex, and the effects of ACTH treatment and a low sodium diet

1998 ◽  
Vol 157 (2) ◽  
pp. 217-223 ◽  
Author(s):  
MM Ho ◽  
GP Vinson
Keyword(s):  
Renin Angiotensin System ◽  
Zona Fasciculata ◽  
Chronic Stimulation ◽  
Angiotensin System ◽  
Sodium Diet ◽  
Adult Rat ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renin Mrna

Transcription of the (pro)renin gene in the adult rat adrenal gland was studied by non-isotopic in situ hybridization. In glands from control (untreated) animals, transcription was relatively sparse, and occurred mostly in the outer zona fasciculata. Treatment with ACTH increased the apparent signal in both the glomerulosa and in fasciculata zones. A low sodium diet initially enhanced the transcription signal specifically in the glomerulosa, but as the regime was extended from 5 days to more than 2 weeks, the signal was also increased dramatically in the zona reticularis. The results emphasize the potential importance of the intraglandular renin-angiotensin system, particularly under conditions of chronic stimulation. They also suggest that angiotensin II, as well as being the major regulator of the glomerulosa, may also have some role in inner adrenocortical zone functions.

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