Control of Aldosterone Secretion

Fraser, Robert; Brown, J. J.; Lever, A. F.; Mason, P A; Robertson, J. I. S.

doi:10.1042/cs0560389

Cited by 109 publications

(35 citation statements)

References 82 publications

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“…Indeed, the mean proportional increment above basal was the same for placebo and both epanolol-treated groups (157, 154 and 141% respectively); only in the atenolol-treated groups was the mean proportional response less (67%). A steepening of the dose-response curve to angiotensin II has been reported for aldosterone in patients with essential hypertension (Fraser et al, 1979). It might be that diminution of basal activity of the renin-angiotensin system by ,B-adrenoceptor blockade further enhanced the response, particularly in the presence of somewhat raised basal serum potassium concentrations (Table 4), another stimulus to aldosterone production.…”

Section: Discussionmentioning

confidence: 98%

Post‐exercise hypotension: the effects of epanolol or atenolol on some hormonal and cardiovascular variables in hypertensive men.

Wilcox

Bennett

Macdonald

et al. 1987

Brit J Clinical Pharma

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Tyne1 Eight men with primary hypertension were treated for 3 weeks with placebo, epanolol (200 mg or 400 mg), or atenolol 100 mg in a randomised cross-over study. Each active treatment period was preceded by a 3 week placebo treatment period and both investigators and subjects were blind to the active drug sequence. 2 At the end of each period, measurements were made of resting cardiovascular (heart rate, blood pressure, forearm blood flow) and biochemical variables (plasma renin, angiotensin II, aldosterone, adrenaline, noradrenaline, vasopressin, sodium and potassium concentrations and osmolality). Responses to exercise (including gas exchange, sweat rate, and ratings of perceived exertion) and the reflex cardiovascular adjustments to distal body subatmospheric pressure were also assessed. 3 The reduction of exercise-induced tachycardia by epanolol 400 mg was comparable to that of atenolol. There was very little difference in the effects of atenolol or epanolol 400 mg on resting blood pressure, but in both cases blood pressures were usually significantly lower than with epanolol 200 mg. 4 Although each active treatment influenced the renin-angiotensin system and circulating levels of catecholamines, the exercise-induced reduction in blood pressure was unaffected. Thus, the hypotensive effects of pharmacological and non-pharmacological interventions were additive.

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Section: Discussionmentioning

confidence: 98%

Post‐exercise hypotension: the effects of epanolol or atenolol on some hormonal and cardiovascular variables in hypertensive men.

Wilcox

Bennett

Macdonald

et al. 1987

Brit J Clinical Pharma

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“…30 In contrast to zona fasciculata function, aldosteroneproducing zona glomerulosa tissue rapidly converts corticosterone to aldosterone, is unable to carry out 17-hydroxylation reactions, and is primarily regulated by ANG II rather than ACTH. 30 It is unlikely, however, that functional separation of the two zones is complete, since zona fasciculata morphology and function are thought to arise from centripetal migration of zona glomerulosa cells. 31 ' 32 A transitional intermediate zone may exist in which cells display biochemical features of both zones.…”

Section: Figure 5 Relationship Between Plasma Concentrations Of Angimentioning

confidence: 99%

Section: Figure 5 Relationship Between Plasma Concentrations Of Angimentioning

confidence: 99%

“…30 Hydroxylation of corticosterone at the 18 position, a putative intermediate step in aldosterone biosynthesis, does not normally occur in the zona fasciculata. 30 In contrast to zona fasciculata function, aldosteroneproducing zona glomerulosa tissue rapidly converts corticosterone to aldosterone, is unable to carry out 17-hydroxylation reactions, and is primarily regulated by ANG II rather than ACTH. 30 It is unlikely, however, that functional separation of the two zones is complete, since zona fasciculata morphology and function are thought to arise from centripetal migration of zona glomerulosa cells.…”

Section: Figure 5 Relationship Between Plasma Concentrations Of Angimentioning

confidence: 99%

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Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia?

Connell¹,

Kenyon²,

Corrie³

et al. 1986

Hypertension

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SUMMARY Dexamethasone-suppressible hyperaldosteronism is a rare familial syndrome in which hypokalemia, suppression of plasma renin concentration, and elevated aldosterone secretion are corrected by treatment with glucocorticoids. Regulation of adrenocortical function and body electrolytes was studied in two affected brothers. Both were hypertensive (210/128 and 160/106 mm Hg) with hypokalemia (3.3 and 3.5 mM) and low plasma renin concentrations. Aldosterone was elevated intermittently with levels as high as 45 ng/dl (normal range, 4-16 ng/dl). Cortisol concentrations were normal but were correlated with aldosterone levels (r = 0.9 and 0.7). Concentrations of 11-deoxycorticosterone (19 and 21 ng/dl; normal range, 4-16 ng/dl) and 18-hydroxycortisol (1000 and 950 ng/dl; normal range, 34-150 ng/dl) were elevated, and diurnal changes in both were the same as those seen with aldosterone. Infusion of adrenocorticotropic hormone,_ 24 (ACTH) caused exaggerated increases of aldosterone, 11-deoxycorticosterone, and 18-hydroxycortisol; cortisol response was normal. A 4-week trial of dexamethasone normalized blood pressure and caused a natriuresis, a fall in aldosterone, and a rise in plasma renin. Administration of ACTH after dexamethasone treatment again caused exaggerated increases of aldosterone. Aldosterone did not respond to angiotensin II before dexamethasone therapy (r = 0.01), but it showed a normal response after therapy (r = 0.8, p<0.01). Neither administration of dopamine (1 /xg/kg/min) nor long-term therapy with bromocriptine (2.5 mg t.i.d. for 4 weeks) affected aldosterone biosynthesis. Thus, loss of dopaminergic inhibition of mineralocorticoid biosynthesis does not account for hyperaldosteronism in this condition. The abnormal pattern of steroid secretion in these brothers is consistent with a population of adrenocortical transition-type cells that secrete aldosterone in response to ACTH but not to angiotensin II and have biosynthetic characteristics of both zona glomerulosa and zona fasciculata cell types. These properties would explain the excess synthesis of 18-hydroxycortisol from a cell type that can uniquely hydroxylate steroid at both the 17 and 18 positions. (Hypertension 8: 669-676, 1986) KEY WORDS • hyperaldosteronism • cortisol • 18-hydroxycortisol 11-deoxycorticosterone * corticosterone EXAMETHASONE-suppressible hyperaldo-I I steronism is a familial form of hypertension A.^^ in which features of mineralocorticoid excess (hypokalemia, low plasma renin concentration) and elevated blood pressure remit during glucocorticoid treatment.13 Basal aldosterone secretion is increased 2 and aldosterone response to adrenocorticotropic hormone (ACTH) is exaggerated, 4 but the exact cause of these biochemical abnormalities, and indeed of the Received September 18, 1985; accepted January 28, 1986. hypertension itself, remains a matter for speculation. 56We studied two brothers with this condition and examined the effect of dexamethasone therapy on body sodium and potassium content. We also examined the effe...

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“…Ang II, a well characterized steroidogenic agent (Fraser et al 1979) elicited a robust 10-fold increase in aldosterone secretion by these cells. The reason why BK, contrary to Ang II, was unable to increase steroidogenesis is probably related to the mechanism of activation utilized by both types of receptors.…”

Section: Discussionmentioning

confidence: 99%

Bovine adrenal glomerulosa cells express such a low level of functional B2 receptors that bradykinin does not significantly increase their aldosterone production

Chrétien

Richard²,

Sn³

et al. 1998

Journal of Endocrinology

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It was recently demonstrated that bradykinin (BK) stimulates aldosterone secretion in bovine adrenal glomerulosa (BAG) cells. The aim of the present study was to characterize the mechanism of action of BK on these cells. ] i which slowly declined to a level that remained above basal level for about 5 min. In the presence of EGTA (2 mM), the rapid and transient calcium increase was unaffected whereas the plateau phase was abolished. Angiotensin II (Ang II, 100 nM) also elicited a typical biphasic response in BAG cells. However the rapid and transient elevation of [Ca 2+ ] i was followed by a sustained plateau phase which remained above the basal level for more than 10 min. Although BAG cells express functional B 2 receptors, no secretion of aldosterone was observed after stimulation with 100 nM BK for 120 min. Under the same conditions Ang II increased by about 10-fold the basal level of aldosterone. The lack of effect of BK is probably attributable to its very transient effect on IP 3 production. Pretreatment of BAG cells with 100 nM BK for 20 min reduced by 70 10% their total binding capacity. These results suggest a rapid and very efficient desensitization process. We conclude that BAG cells express functional B 2 receptors. The weak production of second messengers and the rapid desensitization process could explain why BK fails to increase aldosterone production in these cells. Since functional B 2 receptors are expressed in BAG cells it is likely that under some specific physiological or pathological conditions these receptors may play a significant role in aldosterone secretion. However these conditions remain to be determined.

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Control of Aldosterone Secretion

Cited by 109 publications

References 82 publications

Post‐exercise hypotension: the effects of epanolol or atenolol on some hormonal and cardiovascular variables in hypertensive men.

Post‐exercise hypotension: the effects of epanolol or atenolol on some hormonal and cardiovascular variables in hypertensive men.

Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia?

Bovine adrenal glomerulosa cells express such a low level of functional B2 receptors that bradykinin does not significantly increase their aldosterone production

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