Plasma 4-pregnene-17α,20α-diol-3-one (17α,20α-dihydroxyprogesterone) and 17α-hydroxyprogesterone in man

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Abstract
Investigation of the mechanisms involved in ACTH induced hypertension in sheep led to delineation of the major role of 4-pregnene-17α,20α-diol-3-one (17α,20α-OHP) in ovine adrenal venous blood. It has been shown in this model of steroid induced hypertension that 17α,20α-OHP is ‘hypertensinogenic’ i.e. capable of raising blood pressue when infused concurrently with the major mineralocorticoid and glucocorticoid steroid hormones, but in itself it has no significant blood pressure elevating effect and no significant glucocorticoid or mineralocorticoid activity. The present study examines the regulation of 17α,20α-OHP and 17α-hydroxyprogesterone (17-OHP) in man. The plasma concentration of 17α,20α-OHP in normal ambulant subjects (n = 29) bled at 08.00 to 10.00 h was 14.5 ± 0.8 nmol/l compared with 17-OHP 7.8 ± 0.6 nmol/l. Administration of ACTH (20 μg/kg/day) to normotensive male subjects (n = 6) produced after 5 days of rise in 17α,20α-OHP from 16.6 ± 2.2 to 48.9 ± 7.9 nmol/l and in 17-OHP from 10.9 ± 1.12 to 29.3 ± 4.2 nmol/l. In normal subjects, 17α,20α-OHP had a diurnal rhythm similar to that of cortisol but of lower amplitude. Plasma concentrations of both steroids rose with stepped 30 min ACTH infusions and were suppressed by dexamethasone administration. Angiotensin II infusion, dietary sodium restriction and 9α-fluorocortisol administration had no effect on plasma 17α,20α-OHP. There was no change in 17α,20α-OHP throughout the menstrual cycle but 17-OHP increased during the luteal phase of the cycle. 17-OHP was lower in women on oral contraceptives than in control women, but values for 17α,20α-OHP were unchanged. The mean plasma clearance rate for 17α,20α-OHP in 3 normal subjects was 30.2 l/day/kg, similar to that for aldosterone (31.2 l/day/kg). Unlike the sheep there was no in vitro conversion of 17-OHP to 17α,20α-OHP in human blood. These studies show that 17α,20α-OHP is present in human plasma in higher concentration than 17-OHP. The secretion of 17α,20α-OHP appears to be primarily under the control of ACTH.

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