Stimulation and Suppression of the Mineralocorticoid Hormones in Normal Subjects and Adrenocortical Disorders*

Abstract

Since the identification of aldosterone as the potent salt-retaining and potassium-secreting hormone of the adrenal cortex and being devoid of glucocorticoid properties, the more general term “mineralocorticoid hormone” (MCH) gradually evolved. This term was of particular importance in the clinical arena after the description of primary aldosteronism in 1955. Aldosterone alone was not the sole MCH causing hypertension and renal potassium wasting. Other hypertensive disorders were recognized as either due to deoxycorticosterone (DOC), or the cumulative MCH effect of all steroids of the zona fasciculata (ZF). Disorders of blood pressure and many disorders of potassium metabolism require assessment of the production of MCHs. Additional MCHs, less potent on a molar basis, were soon identified. Their zonal origins and regulation provided new insights into adrenal mechanisms. Maneuvers to stimulate and suppress production of the MCH vary greatly but generally follow attempts to influence the set of the renin-angiotensin or the ACTH-cortisol feedback system. The major MCH in the peripheral circulation is aldosterone, a product of the zona glomerulosa (ZG), and is under primary control of the renin-angiotensin system (RAS) (1). Its precursor, 18- hydroxycorticosterone (18-OHB), though not an effective MCH, also appears in peripheral circulation (2, 3). Earlier aldosterone precursors such as DOC and corticosterone (B) only achieve importance when there is overactivity of this pathway in benign aldosterone-producing adenoma (3, 4).