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

Semple, P. F.; Buckingham, Julia C.; Mason, P A; Fraser, Robert

doi:10.1111/j.1365-2265.1979.tb01359.x

Cited by 38 publications

(15 citation statements)

References 27 publications

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“…In addition, earlier cell-based studies demonstrated that AngII could both stimulate and suppress B production from adrenal cells depending upon the origin of such cells; the stimulatory effect was observed in 'fasciculata-rich' cells and not in total adrenal cells (Spinedi et al 1989). However, a previous small study of human volunteers infused with AngII demonstrated temporary ACTH suppression, which could be in keeping with our results (Semple et al 1979). However, in the latter study, ACTH levels eventually recovered and thus we might have observed a rise in glucocorticoid levels in our subjects if we had extended the sampling time after cessation of infusion.…”

Section: Effect Of Agonists On Corticosteroid Productionsupporting

confidence: 69%

Plasma steroid profiling and response to trophins to illustrate intra-adrenal dynamics

McManus

Fraser

Davies

et al. 2014

Journal of Endocrinology

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The importance of corticosteroids in cardiovascular and other chronic disease is recognised. In addition, plasma steroid precursor-to-product ratios are useful and convenient indirect indicators of efficiency of key steroidogenic enzymes (aldosterone synthase, 11b-hydroxylase and 17a-hydroxylase). The use of liquid chromatography-tandem mass spectrometry (LC-MS/MS) has enabled measurement of numerous corticosteroid compounds simultaneously. However, normal responses to trophins and variation in salt intake are not well described. This study examined these parameters in a large group of healthy volunteers. Sixty normotensive volunteers were recruited and underwent infusion of angiotensin II (AngII) and ACTH, following low-and high-salt diet. Measurement of plasma steroids at baseline and 30 min after infusion of trophin was carried out by LC-MS. As expected, plasma mineralocorticoid levels increased in response to salt restriction and were suppressed with salt loading; ACTH infusion increased all corticosteroids, while AngII increased mineralocorticoids and suppressed glucocorticoid production. ACTH increased S:F but decreased DOC:B, thus the S:F ratio is a more appropriate index of 11b-hydroxylase efficiency. The B:F ratio increased following ACTH treatment and salt restriction. A larger proportion of plasma B than generally accepted may be derived from the zona glomerulosa and this ratio may be most informative of 17a-hydroxylase activity in saltreplete subjects. Although DOC:aldosterone, B:aldosterone and 18-hydroxyB:aldosterone should provide indices of aldosterone synthase efficiency, responses of individual compounds to trophins suggest that none of them accurately reflect this. Based on these data, aldosterone synthase activity is most accurately reflected by aldosterone concentration alone.

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Section: Effect Of Agonists On Corticosteroid Productionsupporting

confidence: 69%

Plasma steroid profiling and response to trophins to illustrate intra-adrenal dynamics

McManus

Fraser

Davies

et al. 2014

Journal of Endocrinology

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“…Neither explanation seems likely, however, since infusion of ACTH causes a brisk increase in aldosterone, often greater than that obtained in normal subjects. 16 Exogenous All inhibits ACTH in normal subjects. 1 ' In a recent study, 14 infusion of ACTH at a low, constant rate restored the response of aldosterone to simultaneously-infused All in Conn's syndrome.…”

Section: Aldosterone and 18-hydroxycorticosteronementioning

confidence: 99%

“…14 Explanations of this poor response, which is well documented, 16 include the autonomous nature of the tumor secretion and a failure of exogenous All to penetrate the steroid-secreting tissue. Neither explanation seems likely, however, since infusion of ACTH causes a brisk increase in aldosterone, often greater than that obtained in normal subjects.…”

Section: Aldosterone and 18-hydroxycorticosteronementioning

confidence: 99%

Response of aldosterone and 18-hydroxycorticosterone to angiotensin II in normal subjects and patients with essential hypertension, Conn's syndrome, and nontumorous hyperaldosteronism.

Fraser¹,

Beretta-Piccoli²,

Brown³

et al. 1981

Hypertension

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SUMMARY Dose-response curves relating plasma angiotensin II (AH) concentration during AH infusion to blood pressure (BP), to plasma aldosterone, and to plasma 18-hydroxycorticosterone were compared in normal subjects and in patients with essential hypertension, Conn's syndrome, and nontumorous hyperaldosteronism. The BP response was steeper than normal in patients with Conn's syndrome and essential hypertension. Before infusion, mean plasma aldosterone concentration was approximately four-fold higher in Conn's syndrome than in the normal group, while that of 18-hydroxycorticosterone was ninefold higher. Neither increased significantly during AH infusion. In essential hypertension, both corticosteroids were within the normal range, but their responses to AH infusion were greater than normal. In the three subjects with nontumorous hyperaldosteronism, plasma aldosterone and 18-hydroxycorticosterone concentrations were raised, and their responses to AH infusion resembled those found in essential hypertension and were different from those found in Conn's syndrome. This suggests that nontumorous hyperaldosteronism is not a rariant of Conn's syndrome. In the response to AH and in other ways, it is indistinguishable from essential hypertension. a benign adrenocortical adenoma (Conn's syndrome), notably ACTH, sodium, and potassium, and hyperaldosteronism associated with bilateral determine the secretion rate and plasma micronodular hyperplasia of the adrenal cortex (nonconcentration of aldosterone in humans, angiotensin tumorous hyperaldosteronism). 2 Data on the behavior II (All) is probably the most important. Angiotensin of 18-hydroxycorticosterone in plasma in these II also raises the plasma concentrations of 18-categories are sparse. The present study compares the hydroxycorticosterone, the probable immediate preeffect of All infusion on plasma concentrations of cursor of aldosterone, but is unimportant in conaldosterone and 18-hydroxycorticosterone in groups trolling the plasma levels of other corticosteroids. In of subjects with these forms of hypertension to its normal subjects, the relationship between plasma All effect in normal subjects, and aldosterone levels can be altered, for example, by sodium depletion or loading: the effect on plasma 18-hydroxycorticosterone concentration is less clear but may also change in this way (see review 1). Methods The All: aldosterone relationship may differ from All subjects were studied under identical conditions normal in some types of hypertension, including essen-, n a metabolic ward. For 5 to 6 days before the study, tial hypertension, primary hyperaldosteronism due to they ate a fixed diet containing between 145 and 155 mEq sodium and between 50 and 80 mEq potassium daily. Angiotensin II (Hypertensin, Ciba) was infused

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“…However, data published thus far do not indicate a direct, causal relationship between AT and cortisol in human models [159] . Data regarding acute effects of AT or angiotensin infusion on HPA axis function are limited, with some studies describing no effect [160,161] , while others report a decrease in ACTH or cortisol secretion [162,163] in humans. Of note, a recent paper by Sanchez-Lemus et al [164] showed that angiotensin II receptor 1A (AT1A) blockade increased basal circulating levels of corticosterone in rats.…”

Section: Angiotensinogen and The Hpa Axismentioning

confidence: 99%

Adipokines and Cardiovascular Risk in Cushing’s Syndrome

et al. 2011

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Cushing’s syndrome (CS) is associated with increased cardiovascular morbidity and mortality. Recent evidence also suggests that increased cardiovascular risk may persist even after long-term remission of CS. Increased central obesity, a typical feature of CS, is associated with altered production of adipokines, which contributes to the pathogenesis of several metabolic and cardiovascular complications observed in this condition. In vitro and in vivo studies have shown a relationship between cortisol and adipokines in several experimental settings. In patients with either active or ‘cured’ CS, an increase in leptin and resistin levels as well as the release of pro-inflammatory cytokines, such as tumor necrosis factor-α and interleukin-6, may be associated with increased cardiovascular risk. For other adipokines, including adiponectin, results are inconclusive. Studies are needed to further elucidate the interactions between clinical and subclinical increases in cortisol production and altered adipokine release in CS.

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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

Cited by 38 publications

References 27 publications

Plasma steroid profiling and response to trophins to illustrate intra-adrenal dynamics

Plasma steroid profiling and response to trophins to illustrate intra-adrenal dynamics

Response of aldosterone and 18-hydroxycorticosterone to angiotensin II in normal subjects and patients with essential hypertension, Conn's syndrome, and nontumorous hyperaldosteronism.

Adipokines and Cardiovascular Risk in Cushing’s Syndrome

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