Recent Progress in the Control of Aldosterone Secretion

Abstract

Publisher Summary This chapter focuses on the recent progress in the control of aldosterone secretion. Aldosterone secretion is regulated by several known mechanisms, including the renin–angiotensin system, adrenocorticotropic hormone (ACTH), and potassium. Additional new mechanisms participate in the control of aldosterone secretion including aldosterone-stimulating factor (ASF) and dopamine. ASF has been purified to homogeneity and determined to be a glycoprotein with a molecular weight of 26,000. The purified glycoprotein, ASF, has a different retention time on HPLC than ACTH, angiotensin II, or s-lipotropin and stimulates aldosterone secretion by a noncyclic AMP-dependent mechanism. ASF-stimulated aldosterone secretion is not blocked by specific competitive antagonists of ACTH or angiotensin II. Fluorescein-labeled antibody in direct measurement has demonstrated ASF in the pituitary gland and in no other tissue. ASF circulates in man. Plasma ASF increases with dietary sodium intake and is not dexamethasone suppressible. Basal plasma and urinary ASF is elevated in idiopathic hyperaldosteronism. Aldosterone secretion is under maximum tonic dopaminergic inhibition. Dopaminergic mechanisms selectively inhibit aldosterone responses to angiotensin II. Dopaminergic suppression of angiotensin II-induced aldosterone secretion is dependent on sodium balance state. ASF and dopamine represent previously unrecognized mechanisms regulating aldosterone secretion in man. Increased secretion of ASF may be responsible for the pathogenesis of idiopathic hyperaldosteronism, and potentially may contribute to other clinical states of aldosterone excess.