Role of the Renin-Angiotensin System in the Regulation of Late Steps in Aldosterone Biosynthesis by Sodium Intake of Potassium-Deficient Rats*

Müller, Jürg; Hofstetter, L.; Schwendener-Canlas, Patricia; Brunner, D. B.; Lund, E

doi:10.1210/endo-115-1-350

Cited by 29 publications

(17 citation statements)

References 33 publications

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“…The adrenal RAS, which is stimulated by low sodium intake , Chiou et al 1995, is thought to enhance the responsiveness of the glomerulosa cells to circulating angiotensin II and results in a maximal increase in aldosterone secretion . This hypothesis supports earlier observations that the prior use of an ACE inhibitor prevents the zona glomerulosa responsiveness to angiotensin II (Müller et al 1984) and the hypertrophy of glomerulosa cells (Mazzocchi & Nussdorfer 1984) in sodium-restricted rats. The present observations certainly support the view that the zona glomerulosa was the main site for (pro)renin synthesis in sodium-restricted rats (Fig.…”

Section: Discussionsupporting

confidence: 92%

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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Section: Discussionsupporting

confidence: 92%

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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“…The circulating angiotensin II level does not appear to be the sole determinant of the adrenal glomerulosa cell response to NaCI restriction, as suggested by the following observations. Chronic infusion of angiotensin II results in a subnormal aldosterone biosynthetic response when compared with the response induced by NaCl restriction (6,36). Anterior pituitary insufficiency is associated with a blunted aldosterone response to NaCl restriction (37)(38)(39).…”

Section: Resultsmentioning

confidence: 99%

Dietary intake of sodium chloride in the rat influences [3H]nitrendipine binding to adrenal glomerulosa cell membranes but does not alter binding to vascular smooth muscle membranes.

Schiebinger¹

1985

J. Clin. Invest.

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Angiotensin II-stimulated secretion by adrenal glomerulosa cells and contraction by vascular smooth muscle (VSM) are dependent on calcium influx through membrane calcium channels. We have examined the hypothesis that the altered responsiveness of adrenal glomerulosa cells and VSM to angiotensin II during NaCl restriction may be associated with a change in membrane calcium channel number. To test this hypothesis, female rats were placed on a high or low NaCl diet. On the 14th day, membranes were prepared from the zona glomerulosa, aorta, mesenteric artery, and uterus. I3HNitrendipine binding was used to monitor calcium channel number. The PHlnitrendipine binding capacity was observed to be higher in the zona glomerulosa during NaCl restriction than during high NaCl intake (83±18 vs. 49±9 fmol/mg protein, P < 0.025, n = 6 paired experiments). The binding capacities of 13Hlnitrendipine on the low and high NaCl diet were similar in the mesenteric artery (10±1 vs. 9±1 fmol/mg protein, n = 8), aorta (33±5 vs. 35±8 fmol/mg protein, n = 5), or uterus (87±15 vs. 85±16 fmol/mg protein, n = 4), respectively. The dissociation constants of PHInitrendipine binding did not differ on a low or high NaCl intake in the zona glomerulosa (0.84±.12 vs. 0.79±.10 nM), mesenteric artery (0.82±.06 vs. 83±.05 nM), aorta (0.90±.11 vs. 0.92±.12 nM), or uterus (0.55±.12 vs. 0.56±.10 nM), respectively. We conclude that the blunted response of VSM to angiotensin II during NaCI restriction is best explained by the previously reported lower number of angiotensin II receptors since calcium channel number does not change. In the adrenal glomerulosa cell, NaCl restriction is associated with a higher number of membrane calcium channels and angiotensin II receptors. The increase in calcium channel number may reflect the influence of an unknown factor(s) believed to be necessary for the full expression of the adrenal glomerulosa cell response to NaCl restriction.

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“…This reinduction had been previously found to be associated with the appearance of a mitochondria1 49-kDa protein, a candidate steroid 18-methyl oxidase catalysing the conversion of corticosterone to 18-hydroxycorticosterone and aldosterone (Meuli & Miiller, 1983a,b). This protein was indeed found to cross-react with an antibody raised against bovine adrenal cytochrome P-4501 (Miiller et al, 1989).…”

Section: Aldosterone Synthase Effectsmentioning

confidence: 93%

“…They further found that inhibition of angiotensin converting enzyme did not affect aldosterone biosynthesis in rats with established combined sodium and potassium deficiency, but blocked the stimulation of the conversion of corticosterone to 18-hydroxycorticosterone and aldosterone by sodium restriction in potassium depleted rats (Miiller et al, 1984). Thus the sensitivity of the zona glomerulosa to long-term stimulation by angiotensin I1 depends on sodium intake, and thus the renin-angiotensin system, and appears also to be regulated by the plasma potassium levels.…”

Section: In-vivo Anlmal Studlesmentioning

confidence: 96%

“…Although earlier clinical studies in humans pointed to a site of stimulation of aldosterone biosynthesis by angiotensin I1 and potassium prior to the formation of desoxycorticosterone (Brown et ul., 1972), in-vitro studies with dispersed glomerulosa cells derived from the adrenal glands of humans (Williams & Braley, 1977) or rats (Miiller et al, 1984) subjected in vivo to sodium restriction or potassium loading underlined the importance of stimulation of the late steps of aldosterone biosynthesis. This fact was reinforced more recently by Tremblay et al (1992) who demonstrated that potassium supplementation or sodium restriction in rats increased aldosterone synthase but not 1 ID-hydroxylase P-450 mRNA.…”

Section: Aldosterone Synthase Effectsmentioning

confidence: 99%

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Potassium‐angiotensin interplay in the regulation of aldosterone biosynthesis

1995

Clinical Endocrinology

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Although the biosynthesis of aldosterone in the zona glomerulosa of the adrenal cortex is known to be regulated by a whole array of other agents (ACTH, serotonin, dopamine, atrial natriuretic peptide, acetylcholine) (Miiller, 1988) in this short review we will concentrate on the interplay between the two major regulators, angiotensin I1 and potassium ion ( K ' ) . For many years, specific diseases as well as pathophysiological clinical situations have taught us much about the relation between the renin-angiotensin system and potassium, which has been further explored by animal experimentation. More recently, considerable progress has been achieved in our understanding of the mode of action of both angiotensin I1 and K+ at the cellular level, putting their interplay into a new light. Clinical obsewatlonsThere are many diseases and clinical settings which are caused by abnormalities of secretion of one or other member of the renin-angiotensin system and of the mineralocorticoid family of compounds, mainly aldosterone, or in which these hormones react to or adapt to disturbances of potassium economy. The latter is easily disturbed, which is not surprising given that the total potassium available in the extracellular fluid is 65 mmol, compared with some 5 mol of intracellular potassium. This is distributed mainly in muscle (approximately 2650 mmol), with the erythrocytes, liver and bones each accounting for approximately 250-300 mmol. The turnover of body potassium reflects a daily intake of approximately 100 mmol in the diet, and equivalent excretion mainly by the kidney and to a smaller extent in the stool.In circumstances under which the renin-angiotensin system is primarily stimulated, secondary hyperaldosteronCorrespondence: Professor M.

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Role of the Renin-Angiotensin System in the Regulation of Late Steps in Aldosterone Biosynthesis by Sodium Intake of Potassium-Deficient Rats*

Cited by 29 publications

References 33 publications

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

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

Dietary intake of sodium chloride in the rat influences [3H]nitrendipine binding to adrenal glomerulosa cell membranes but does not alter binding to vascular smooth muscle membranes.

Potassium‐angiotensin interplay in the regulation of aldosterone biosynthesis

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