Literature DB >> 190252

Response of several adrenal steroids to ACTH stimulation in essential hypertension.

M Honda, W Nowaczynski, G P Guthrie, F H Messerli, G Tolis, O Kuchel, J Genest.   

Abstract

Plasma concentrations of progesterone (P), deoxycorticosterone (DOC), 17-hydroxyprogesterone (17-OH P), corticosterone (B), deoxycortisol (S), cortisol (F), and aldosterone were measured in 8 control subjects and in 10 patients with low and normal renin essential hypertension (EH) before and 4 and 8 h after an iv infusion of 25 units of ACTH. Secretion rates of 18-hydroxy-11-deoxycorticosterone (18-OH DOC) were measured for the 24 h prior to and the day of the ACTH infusions. The hypertensive patients had significantly higher plasma levels of aldosterone, DOC and S after ACTH than the controls, whereas plasma B levels were significantly lower. The low renin subgroup considered separately had significantly higher plasma levels of aldosterone and DOC than controls, and higher levels of B and lower levels of F than the normal renin subgroup in response to ACTH. Although not significantly different, the plasma levels of P and the secretion rate of 18-OH DOC tended to be higher, and plasma 17-OH P and F levels lower after ACTH in patients with EH than in controls. The low renin subgroup tended to have the highest plasma S levels and 18-OH DOC secretory rates and lowest F levels. Estimations of adrenal 11beta-hydroxylating efficiency in response to ACTH in patients and controls by plasma steroid ratios revealed significantly lower B/DOC ratios in both low and normal renin patients compared to controls, supported by somewhat lower F/S ratios in these patients, especially those in the low renin subgroup. Altered 17-hydroxylating efficiency seen by significantly lower 17-OH P/P ratios were also found in those with EH, supported by somewhat lower F/B and S/DOC ratios in these patients, agian especially in the low renin subgroup. These data are compatible with a pattern of altered adrenocortical steroid biosynthesis in essential hypertension bearing features similar to adrenal 11beta and 17alpha-hydroxylation deficiencies.

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Year:  1977        PMID: 190252     DOI: 10.1210/jcem-44-2-264

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  4 in total

Review 1.  Mechanisms of hypertension: the expanding role of aldosterone.

Authors:  E Marie Freel; John M C Connell
Journal:  J Am Soc Nephrol       Date:  2004-08       Impact factor: 10.121

2.  [On the ACTH-corticoid relation in essential hypertension in dependence of plasma-renin activity (PRA) (author's transl)].

Authors:  T Hossdorf; F Wessels; H Wagner; B Eienbröker; R Kleimann; G Degenhardt
Journal:  Klin Wochenschr       Date:  1978-05-01

3.  Low-renin primary hypertension in a young patient treated with dexamethasone.

Authors:  A P Tommaselli; G De Simone; L Di Lorenzo; R Rossi; A Cocca; R Valentino; B Biondi; G Lombardi
Journal:  J Endocrinol Invest       Date:  1986-02       Impact factor: 4.256

4.  A pilot study for neonatal screening of congenital adrenal hyperplasia due to 21-hydroxylase and 11-beta-hydroxylase deficiency in Campania region.

Authors:  R Valentino; A P Tommaselli; R Rossi; G Lombardi; S Varrone
Journal:  J Endocrinol Invest       Date:  1990-03       Impact factor: 4.256

  4 in total

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