The regulation of plasma 18-hydroxy 11-deoxycorticosterone in man.

Abstract

A B S T R A C T 18-hydroxy 11-deoxycorticosterone (18-OH DOC), a weak mineralocorticoid, was estimated by a radioimmunoassay procedure after purification in 49 patients with hyper,tension and 38 normal control subjects. The sensitivity of the method was 2-4 pg; there was no detectable blank, and the precision was 9-10%. In normal subjects the absolute plasma levels were similar to those of aldosterone. ACTH administration produced a 23-fold increase, and sodium restriction resulted in a 4-fold increase (5.4+-0.7-20.5±3.0 ng/dl). On the other hand, the plasma levels of 18-OH DOC declined by nearly 50% with upright posture or angiotensin II infusion. During both of these procedures, plasma aldosterone levels significantly increased. Patients with normal and low renin hypertension had similar changes in plasma 18-OH DOC levels with sodium restriction. However, the mean high sodium level in the normal renin essential hypertension group (11.6±-1.6 ng/dl) was significantly greater (P < 0.001) than in the control group (5.4±0.7 ng/dl). In addition, at least 22% and perhaps as high as 37% of the hypertensive subjects had levels greater than the upper limits of normal on a high sodium intake. Differences between the groups were less impressive in the sodiumrestricted studies. There were no significant differences in age, duration of hypertension, sodium balance, serum sodium, potassium, or blood urea nitrogen in those patients who had elevated levels of plasma 18-OH DOC. Patients with primary aldosteronism had levels within -the normal range on both dietary intake. However, in contrast to the other groups there were no significant changes in the plasma levels with sodium restriction. Thus, a significant number of patients with essential hypertension presumably have an alteration in 18-OH DOC secretion.

Effect of Uni-adrenalectomy on Blood Pressure in a Patient with Excessive Adrenal 18-hydroxy-11-deoxycorticosterone Production Bilaterally

“…These regulations correspond to those appearing in normal subjects and patients with essential hypertension (13,14) except that the patient excessively secreted 18-OH-DOCfrom adrenal glands in response to ACTH. Although the adrenal mass was diagnosed as nonfunctional, there remained a possibility that this mass was malignant because a mass larger than 4 cm in diameter has a high probability of being malignant (15 Wealso measuredABPM on two occasions each before and after adrenalectomy because a single ABPM has been reported to be unreliable for determining the magnitude of the nocturnal decline in BP (18).…”

Plasma concentrations of 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone simultaneously measured in normal subjects and adrenocortical disorders.

“…Certain authors (Martin et al 1975, Chandler et al 1976Williams et al 1976;Ojima et al 1978) measured individual plasma levels of 18-OH-DOC and 18-OH-B, but few evaluated these two steroids simultaneously in the single extract. The major problems for establishing this procedure may be the following three: effective separation of the steroids, adequate purification, and sufficiently sensitive quantitation.…”

Partial deficiency of adrenal 11-hydroxylase. A possible cause of primary hypertension.

“…High plasma levels of 18-OHDOC also have been reported in patients with normal-renin hypertension. 4 The capability of deoxycorticosterone (DOC) to induce hyper- Received March 9, 1984; revision accepted September 24, 1984. tension has been demonstrated by McCall and coworkers 5 in rats treated with methylandrostenediol. Dexamethasone has also been used recently in hypertensive patients with excessive secretion of an unknown mineralocorticoid 6 and in a hypertensive girl with excessive secretion of urinary 17-ketosteroids.…”