Role of 18-hydroxy-11-deoxycorticosterone and 16 alpha, 18-dihydroxy-11-deoxycorticosterone in hypertension.
Excess secretion of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) occurs in more than 10% of hypertensive patients with suppressed plasma renin activity, but it also is reported to occur in essential hypertension without impairment of the renin system. Preliminary studies measuring plasma 18-OH-DOC by radioimmunoassay support the idea that 18-OH-DOC secretion is elevated in some patients with essential hypertension. Interpretation of these data must take into account endogenous ultradien and circadian variations in plasma 18-OH-DOC, however. 18-OH-DOC serves as a precursor of another steroid secretory product. Conversion of labeled 18-OH-DOC to a new structure, 16alpha, 18-dihydroxy-11-deoxycorticosterone (16alpha, 18-diOH-DOC), was demonstrated to be greatly accelerated by the adrenal tissue in low-renin patients as compared with those with normal adrenal tissue (70 to 80% versus 15% conversion). Hypersecretion of 16alpha, 18-diOH-DOC occurred in each. This steroid exerted no effect on sodium metabolism in adrenalectomized rats or in the toad bladder assay, but it markedly enhanced activity of subthreshold doses of aldosterone in reducing sodium excretion in urine of adrenal-ectomized rats. Because of the unique activity of this steroid, we have concluded that excessive 16alpha, 18-diOH-DOC secretion may be important in the genesis of suppressed renin in some patients with hypertension.
D015070:18-Hydroxydesoxycorticosterone / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism* / Q000652:urine; D000302:Adrenal Cortex / Q000378:metabolism; D002940:Circadian Rhythm; D003900:Desoxycorticosterone / Q000031:analogs & derivatives*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D012083:Renin / Q000097:blood
D015070:18-Hydroxydesoxycorticosterone; D003900:Desoxycorticosterone; D012083:Renin