Serotoninergic stimulation of aldosterone secretion in the rat in vivo: role of the renin-angiotensin system

1991 ◽  
Vol 130 (3) ◽  
pp. 347-355 ◽  
Author(s):  
E. Davies ◽  
S. Rossiter ◽  
C. R. W. Edwards ◽  
B. C. Williams

ABSTRACT Serotoninergic control of aldosterone secretion in vivo was investigated in conscious rats with indwelling arterial cannulae. Serial blood samples were taken from the animals before and after i.p. administration of 1 ml (4 g/l) 5-hydroxytryptophan (5-HTP), the precursor of serotonin, or saline and they were analysed for 5-HTP, serotonin, 5-hydroxyindoleacetic acid, plasma renin activity (PRA), corticosterone, aldosterone, sodium and potassium concentrations. The role of the renin-angiotensin system was investigated in animals pretreated for 1 week with the angiotensin-converting enzyme inhibitor captopril (25 mg/day). 5-HTP caused a significant increase in all parameters within 45 min except for sodium and potassium. Saline administration showed no significant effect. Captopril pretreatment did not impair the increase in any parameter by 5-HTP, with the exception of the aldosterone response which was significantly attenuated, though not completely. The results show that administration of 5-HTP, which increases serum serotonin levels, stimulates PRA, aldosterone and corticosterone secretion. Captopril pretreatment inhibits the aldosterone response, suggesting that the aldosterone stimulatory properties of 5-HTP require the presence of angiotensin II, although it is unclear whether it acts in a mediatory or permissive capacity. The failure of captopril to inhibit the aldosterone response completely suggests the involvement of other mechanisms such as the hypothalamo-pituitary adrenal axis or a direct action of serotonin on the adrenal. Journal of Endocrinology (1991) 130, 347–355

2000 ◽  
Vol 278 (6) ◽  
pp. E1027-E1030 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Ludwik K. Malendowicz ◽  
Anna Markowska ◽  
Giovanna Albertin ◽  
Gastone G. Nussdorfer

This study examined the effect of the pharmacological manipulation of adrenal renin-angiotensin system (RAS) on aldosterone secretion from in situ perfused adrenals of rats kept on a normal diet and sodium restricted for 14 days. Neither the angiotensin-converting enzyme inhibitor captopril nor the nonselective angiotensin II receptor antagonist saralasin and the AT1 receptor-selective antagonist losartan affected basal aldosterone output in normally fed rats. In contrast, they concentration dependently decreased aldosterone secretion in sodium-restricted animals, with maximal effective concentration ranging from 10− 7 to 10− 6 M. Captopril (10− 6 M), saralasin (10− 6 M), and losartan (10− 7 M) counteracted aldosterone response to 10 mM K+ in sodium-restricted rats but not in normally fed animals. Collectively, these findings provide evidence that adrenal RAS plays a role in the regulation of aldosterone secretion, but only under conditions of prolonged stimulation of zona glomerulosa probably leading to overexpression of adrenal RAS.


1982 ◽  
Vol 243 (1) ◽  
pp. E48-E51 ◽  
Author(s):  
H. Suzuki ◽  
M. Handa ◽  
K. Kondo ◽  
T. Saruta

The role of the renin-angiotensin system in the regulation of the blood pressure of dexamethasone-treated rats (Dex) was evaluated using saralasin, an angiotensin II antagonist, and SQ 14225 (SQ) (d-3-mercapto-2-methylpropranoyl-1-proline), an angiotensin-converting enzyme inhibitor. During a 7-day period blood pressure rose 65 +/- 10 mmHg (P less than 0.001) in Dex with no significant changes in plasma renin activity. Concurrent administration of dexamethasone and SQ attenuated the elevation of blood pressure (P less than 0.05). In the conscious, freely moving state, intravenous injection of SQ (10, 30, 100 micrograms/kg) reduced blood pressure of DEX in a dose-dependent manner (P less than 0.05). Also, intravenous injection of saralasin (10 micrograms.kg-1 . min-1) reduced blood pressure significantly (P less than 0.01). Bilateral nephrectomy abolished the effects of saralasin and SQ on blood pressure in Dex. These results indicate that the elevation of blood pressure in DEX depends partially on the renin-angiotensin system.


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.


1990 ◽  
Vol 122 (3) ◽  
pp. 369-373 ◽  
Author(s):  
Hiroyuki Sasamura ◽  
Hiromichi Suzuki ◽  
Ryuichi Kato ◽  
Takao Saruta

Abstract Angiotensin II, ACTH and potassium chloride were administered to rats for 6 days and the effects on adrenal renin-like activity and adrenal angiotensin II/III immunoreactivity were investigated. Rats infused with angiotensin II(140 pmol/min) either ip or sc showed increases in adrenal angiotensin II/III immunoreactivity (p<0.05) and plasma aldosterone concentration (p<0.05), but no change in adrenal renin-like activity. Captopril treatment of angiotensin Il-infused rats caused a slight decrease in angiotensin II/III immunoreactivity which did not reach statistical significance. In contrast, rats treated with ACTH (Cortrosyn-Z, 3 IU/day, sc) showed an increase in adrenal renin-like activity (p<0.01), but no significant change in adrenal angiotensin II/III immunoreactivity. Rats treated with KCl in drinking water showed increases (p<0.05) in adrenal renin-like activity, adrenal angiotensin II/III immunoreactivity, and plasma aldosterone. These results suggest that angiotensin II, ACTH and potassium, three major regulators of aldosterone secretion by the adrenal gland, have different effects on the adrenal renin-angiotensin system when administered in vivo.


2020 ◽  
Vol 106 (1) ◽  
pp. e45-e60
Author(s):  
Matthieu St-Jean ◽  
Isabelle Bourdeau ◽  
Marc Martin ◽  
André Lacroix

Abstract Context In primary aldosteronism (PA), aldosterone secretion is relatively independent of the renin–angiotensin system, but can be regulated by several other stimuli. Objective To evaluate aldosterone response to several stimuli in a series of patients with PA secondary either to bilateral adrenal hyperplasia (BAH) or unilateral aldosterone-producing adenoma (APA). Design and setting Prospective cohort study conducted in a university teaching hospital research center. Patients Forty-three patients with confirmed PA and subtyped by adrenal vein sampling (n = 39) were studied, including 11 with BAH, 28 with APA, and 4 with undefined etiology. We also studied 4 other patients with aldosterone and cortisol cosecretion. Interventions We systematically explored aberrant regulation of aldosterone using an in vivo protocol that included the following stimulation tests performed over 3 days under dexamethasone suppression: upright posture, mixed meal, adrenocorticotropin (ACTH) 1-24, gonadotropin-releasing hormone (GnRH), vasopressin, and serotonin R4 agonist. Main outcome measures Positive response was defined as &gt;50% renin or ACTH-independent increase in plasma aldosterone/cortisol concentration following the various stimulation tests. Results Renin-independent aldosterone secretion increased in response to several aberrant stimuli (upright posture, GnRH) in up to 83% of patients with APA or BAH in whom ACTH 1-24 and HT4R agonists also produced aldosterone oversecretion in all patients. The mean significant aberrant responses per patient was similar in BAH (4.6) and in APA (4.0). Conclusions Aldosterone secretion in PA is relatively autonomous from the renin–angiotensin system, but is highly regulated by several other stimuli, which contributes to the large variability of aldosterone levels in PA patients.


Thorax ◽  
2007 ◽  
Vol 62 (6) ◽  
pp. 527-535 ◽  
Author(s):  
J.-S. Jerng ◽  
Y.-C. Hsu ◽  
H.-D. Wu ◽  
H.-Z. Pan ◽  
H.-C. Wang ◽  
...  

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