Effect of atrial peptides on aldosterone production.

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Abstract

This study examines the effects of the synthetic atrial peptides (atriopeptin I, II, and III) on aldosterone and corticosterone production by rat adrenal cell suspensions. Furthermore, we studied the effect of atriopeptin II infusion on the plasma aldosterone response to angiotensin II in the rat in vivo. Atriopeptin I, II, and III decreased aldosterone release from zona glomerulosa cells in a dose-dependent fashion. 10 pM atriopeptin II inhibited basal aldosterone release significantly (P less than 0.01), and 10 nM atriopeptin II or III lowered it by 79%. Atriopeptin II decreased the sensitivity of the glomerulosa cells to adrenocorticotropic hormone (ACTH) and angiotensin II. Atriopeptin II had no effect on basal or ACTH-stimulated corticosterone release by fasciculata-medullary cells. In vivo infusions of angiotensin II with or without simultaneous infusions of atriopeptin II showed that atriopeptin II significantly inhibited the aldosterone response to angiotensin II. This inhibition by atriopeptin II was independent of any effect on plasma renin activity, serum potassium, or ACTH. These data raise the possibility that the atrial natriuretic peptides may affect sodium excretion by the kidney, not only directly, but also indirectly through the inhibition of aldosterone production.

Authors

K Atarashi, P J Mulrow, R Franco-Saenz