Combined effects of angiotensin II and ACTH on cortisol production: In vitro studies on isolated guinea-pig adrenal cells

Pham-Huu-Trung, M T; Lombès, Marc; Bogyo, A.; Girard, François

doi:10.1016/0022-4731(81)90242-9

Cited by 14 publications

(2 citation statements)

References 27 publications

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“…This result agrees with previous ones [20,27,39] and confirms that AII exerts a trophic effect on the rat zona fasciculata [38], which is the main producer of corticosterone in Rodentia [43]. However, this effect of AII seems to be of moderate dimension and doubtful physiological sig-nificance, inasmuch as CP does not appear to affect the steroidogenic capacity of the zona fasciculata (i.e., corticosterone output).…”

Section: Trophic Effects Of the Renin-angiotensin System And The Sodisupporting

confidence: 94%

Investigations on the possible involvement of the dopaminergic system in the modulation of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa: A coupled morphometric and biochemical study

et al. 1987

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The effects of metoclopramide (MTC) and bromocriptine (BRC) (two drugs which act as antagonist and agonist of DOPA-receptors, respectively) on the zona glomerulosa of dexamethasone/ACTH-treated rats were investigated by coupled biochemical and morphometric techniques. Short-term (1-h) MTC administration significantly increased the plasma concentration of aldosterone, while long-term (7-day) MTC administration, as well as short- and long-term treatment with BRC did not cause any apparent change. Long-term MTC administration was found to significantly potentiate both the rise in the plasma level of aldosterone and the hypertrophy of the zona glomerulosa and its parenchymal cells induced by a prolonged treatment with angiotensin II (AII), but not those evoked by a chronic sodium deprivation alone or combined with AII infusion. Long-term BRC administration notably counteracted the effects of sodium restriction (coupled or not with AII infusion), but not those induced by the administration of AII alone. Long-term MTC administration partially reversed both the lowering of the plasma concentration of aldosterone and the atrophy of the zona glomerulosa and its parenchymal cells caused by a prolonged sodium-loading (combined or not with captopril infusion), but not those produced by the administration of captopril alone. On the other hand, long-term BRC treatment induced a further significant reduction in the blood level of aldosterone and the volume of zona glomerulosa and its cells only in captopril-treated animals. These findings are consistent with the view that the dopaminergic system exerts a maximal tonic inhibitory effect not only on the secretory activity, but also on the growth and steroidogenic capacity of the rat zona glomerulosa. Furthermore, they suggest that the activity of the dopaminergic system is in turn controlled by the sodium balance, being almost completely suppressed by a prolonged sodium deprivation.

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Section: Trophic Effects Of the Renin-angiotensin System And The Sodisupporting

confidence: 94%

Investigations on the possible involvement of the dopaminergic system in the modulation of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa: A coupled morphometric and biochemical study

et al. 1987

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“…Although the significance of the local RAS in the adrenal inner cortex receives very little attention, it has been shown that long-term angiotensin II administration slightly stimulates the growth of the rat zona fasciculata, and increases plasma corticosterone concentration in vivo (Nussdorfer et al 1981, Mazzocchi et al 1985. Other reports also demonstrated that angiotensin II enhances the secretory activity of fasciculata cell preparations in other species in vitro (Hepp et al 1977, McKenna et al 1978, Pham-Huu-Trung et al 1981, while McEwan et al (1996) showed that angiotensin II, like a low sodium diet, increased cell proliferation in the reticularis as well as in the glomerulosa. It is, of course, well documented that angiotensin II is a specific zona glomerulosa stimulant and an important regulator of aldosterone secretion in most mammalian species (Glöz & Sugar 1962, Müller 1988).…”

Section: Discussionmentioning

confidence: 99%

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

Ho¹,

Vinson²

1998

Journal of Endocrinology

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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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Angiotensin II and glucocorticoid release: Direct effect at the adrenal level and modulation of the adrenocorticotropin-induced glucocorticoid release

Spinedi¹,

Aguado

Basilotta³

et al. 1989

J Endocrinol Invest

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Angiotensin II (A II) stimulates adrenal glomerulosa cells releasing mineralocorticoids; however, little is known about the A II effect on glucocorticoids output. The present study has been designed in order to see if A II could modify in vitro spontaneous and ACTH-induced corticosterone (B) release from both fasciculata-reticularis enriched and total adrenal cells. The results indicate that A II at 10(-12), 10(-11), 10(-10) and 10(-6) M concentrations did not modify basal B production and A II 10(-9), 10(-8) and 10(-7) M decreased basal B production from total adrenal cells. Whereas A II (10(-10)-10(-6) M) stimulated B release from fasciculata-reticularis enriched cells. On the one hand, 10(-8) M A II significantly decreased ACTH-elicited B release from total adrenal cells; effect completely abolished by saralasin (SAR, 10(-8) M), a specific A II receptor blocker. On the other hand, 10(-8) M A II did not modify ACTH-induced B release from fasciculata-reticularis enriched cells. Finally, 10(-10) to 10(-6) M A II and 22 pM ACTH stimulated aldosterone output from total adrenal cells; while, fasciculata-reticularis enriched cells did not secrete any measurable amount of aldosterone under basal condition and after incubation with A II. These data further suggest a regulatory role of A II in the release of glucocorticoids from the adrenal gland.

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Combined effects of angiotensin II and ACTH on cortisol production: In vitro studies on isolated guinea-pig adrenal cells

Cited by 14 publications

References 27 publications

Investigations on the possible involvement of the dopaminergic system in the modulation of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa: A coupled morphometric and biochemical study

Investigations on the possible involvement of the dopaminergic system in the modulation of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa: A coupled morphometric and biochemical study

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

Angiotensin II and glucocorticoid release: Direct effect at the adrenal level and modulation of the adrenocorticotropin-induced glucocorticoid release

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