Aldosterone Regulation in Sodium Deficiency: Role of Ionic Factors and Angiotensin II

Blair‐West, J. R.; Coghlan, John P.; Denton, D. A.; Scoggins, Bruce A.

doi:10.1007/978-3-642-65600-2_18

Cited by 11 publications

(4 citation statements)

References 118 publications

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“…Angiotensin 11, infused into normal subjects in amounts which raise its blood concentration t o levels within the physiological range, increases the plasma concentration of aldosterone and 18-hydroxycorticosterone (Mason et al, 1976a), but does not influence the circulating levels of other corticosteroids. It has been proposed that angiotensin I1 stimulates corticosteroid biosynthesis early in the pathway (Muller, 1971;Blair-West et al, 1974) and the lack of response of deoxycorticosterone (DOC), corticosterone, cortisol or 18-hydroxy DOC in vivo t o infused angiotensin I1 is therefore surprising.…”

Section: S U M M a R Ymentioning

confidence: 99%

“…It could be a direct effect of the infused angiotensin on the brainhypothalamus-pituitary complex or an effect on the metabolism of ACTH.Angiotensin 11, infused into normal subjects in amounts which raise its blood concentration t o levels within the physiological range, increases the plasma concentration of aldosterone and 18-hydroxycorticosterone (Mason et al, 1976a), but does not influence the circulating levels of other corticosteroids. It has been proposed that angiotensin I1 stimulates corticosteroid biosynthesis early in the pathway (Muller, 1971;Blair-West et al, 1974) and the lack of response of deoxycorticosterone (DOC), corticosterone, cortisol or 18-hydroxy DOC in vivo t o infused angiotensin I1 is therefore surprising.Recently it has been shown that the simultaneous infusion of angiotensin I1 and corticotrophin (ACTH) increases not only the plasma concentrations of aldosterone and 18hydroxy corticosterone but also those of cortisol, DOC, corticosterone and 18-hydroxy DOC (Mason et al, 1976b;. This suggested that ACTH is necessary for the full steroidogenic response and that ACTH release may have been inhibited in subjects infused with angiotensin I1 alone.…”

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confidence: 99%

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SUPPRESSION OF PLASMA ACTH CONCENTRATION BY ANGIOTENSIN II INFUSION IN NORMAL HUMANS AND IN a SUBJECT WITH a STEROID 17α‐HYDROXYLASE DEFECT

Semple¹,

Buckingham²,

Mason³

et al. 1979

Clinical Endocrinology

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Six healthy subjects were infused with angiotensin II and plasma concentrations of angiotensin, ACTH and cortisol were measured before, during and after the infusion. In all cases the plasma ACTH concentration fell as plasma angiotensin increased and rose again, sometimes to higher than basal levels, when the angiotensin infusion was terminated. These effects were most marked at the highest rate of infusion (8 pmol/kg/min) and, at the lower rates (2 and 4 pmol/kg/min), there was some recovery of ACTH levels during the infusion period in some subjects. Plasma ACTH concentrations also fell when angiotensin was infused into a patient with high ACTH levels due to a steroid 17 alpha-hydroxylation defect. The inhibition of ACTH secretion is not due to a rise in plasma cortisol operating a negative feedback inhibition. It could be a direct effect of the infused angiotensin on the brain-hypothalamus-pituitary complex or an effect on the metabolism of ACTH.

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Section: S U M M a R Ymentioning

confidence: 99%

mentioning

confidence: 99%

SUPPRESSION OF PLASMA ACTH CONCENTRATION BY ANGIOTENSIN II INFUSION IN NORMAL HUMANS AND IN a SUBJECT WITH a STEROID 17α‐HYDROXYLASE DEFECT

Semple¹,

Buckingham²,

Mason³

et al. 1979

Clinical Endocrinology

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“…However, the effects are different in the two main target-organs of the hormone: sodium restriction increases the steroidogenic effect and decreases the myotropic and vasopressor action of angiotensin I1 (Strewler, Hinrichs, Guiod & Hollenberg, 1972;Blair-West, Coghlan, Denton & Scoggins, 1974;Spielman & Davis, 1974;Williams, Hofienberg & Braley, 1976;Slack & Ledingham, 1977;Aguilera, Hauger & Catt, 1978); sodium loading has the opposite effect. The biological effect of a peptide hormone such as angiotensin I1 results from a series of complex intracellular events initiated by the specific recognition of the hormone by membrane receptors.…”

Section: Introductionmentioning

confidence: 99%

Alterations of Adrenal and Uterine Angiotensin II Receptors during Variation of Sodium Intake and/or Experimental Hypertension

et al. 1978

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1. Angiotensin I1 receptors from rat adrenal gland and myometrium were studied during variation of sodium intake.2. In both target-tissues low Na+ diet increased the number of receptors whereas a high Na+ diet did not modify the adrenocortical receptors but increased the number of uterine receptors.3. Deoxycorticosterone and one kidney Goldblatt hypertension were associated with a decrease in the number of adrenal receptors.4. Alterations of angiotensin I1 receptors alone cannot explain satisfactorily the variations of sensitivity of target-cells to angiotensin I1 during sodium balance changes.

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“…The production of aldosterone by the zona glomerulosa of the adrenal cortex during changes in electrolyte balance is believed to be controlled predominantly by the circulating levels of angiotensin II and by the extracellular concentrations of potassium and sodium (1,2). Aldosterone production is also influenced by ACTH, but the role of this peptide under physiological conditions is probably minor.…”

Section: Introductionmentioning

confidence: 99%

Regulation of angiotensin II receptors in the rat adrenal cortex by dietary electrolytes.

Douglas¹,

Catt²

1976

J. Clin. Invest.

134

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A B S T R A C T The binding affinity and concentration of specific angiotensin II receptor sites of rat adrenal cortical cells and homogenates were determined after 1 and 6 wk of altered sodium and potassium intake. Sodium deprivation caused marked increases in plasma renin, blood angiotensin II, and plasma aldosterone, and was accompanied by a significant increase (+ 74%) in the number of specific angiotensin II receptor sites per adrenal cortical cell. High potassium intake was followed by increased serum potassium and markedly elevated plasma aldosterone, with subnormal levels of renin and angiotensin II and a 170% increase in the number of angiotensin II receptors per cell after 1 wk. Sodium loading and potassium deprivation were followed by the opposite effect upon adrenal receptors, with reduction of the angiotensin II-binding capacity. None of the dietary electrolyte changes were accompanied by an increase in receptor affinity above the control value of 2 nM'. A decrease in receptor affinity was noted after 6 wk of either low sodium or low potassium intake, when the renin and angiotensin II levels were increased by 104-129%.The adrenals of normal rats infused acutely with synthetic angiotensin II, or anesthetized with ether or sodium pentobarbital, which markedly increased plasma renin activity, contained fewer angiotensin receptors. These reductions in binding site concentration were not accompanied by changes in affinity and were attributed to occupancy by angiotensin II.These studies have demonstrated that chronic changes in sodium or potassium balance and acute changes in blood angiotensin II levels can exert modulating effects upon the adrenal content and/or affinity of specific receptor sites for angiotensin II.

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Aldosterone Regulation in Sodium Deficiency: Role of Ionic Factors and Angiotensin II

Cited by 11 publications

References 118 publications

SUPPRESSION OF PLASMA ACTH CONCENTRATION BY ANGIOTENSIN II INFUSION IN NORMAL HUMANS AND IN a SUBJECT WITH a STEROID 17α‐HYDROXYLASE DEFECT

SUPPRESSION OF PLASMA ACTH CONCENTRATION BY ANGIOTENSIN II INFUSION IN NORMAL HUMANS AND IN a SUBJECT WITH a STEROID 17α‐HYDROXYLASE DEFECT

Alterations of Adrenal and Uterine Angiotensin II Receptors during Variation of Sodium Intake and/or Experimental Hypertension

Regulation of angiotensin II receptors in the rat adrenal cortex by dietary electrolytes.

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