B J Ballermann, K D Bloch, J G Seidman, B M Brenner
J Clin Invest.
1986;
78(3):840–843
doi:10.1172/JCI112650
This article Copyright © 1986, The American Society for Clinical Investigation
Abstract
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T
he mechanisms that mediate renal "escape" from the sodium-retaining effects of mineralocorticoids are incompletely understood. This study was undertaken to determine whether atrial natriuretic peptide (ANP) may play a role in the escape phenomenon. Immunoreactive ANP in rat plasma increased 2.5-fold above baseline values at 12 and 24 h after a single depot injection of desoxycorticosterone acetate in oil and returned to baseline thereafter. In addition, specific pre-pro-ANP messenger RNA content in rat atria was significantly elevated as early as 12 h after mineralocorticoid administration and remained elevated at 24, 48, and 72 h, indicating a prompt and sustained increase in ANP biosynthesis. Renal glomerular ANP receptor density was down-regulated appropriately with rising plasma ANP levels, and receptor affinity was unchanged. Thus, mineralocorticoid administration in the rat is a powerful stimulus for ANP release and for atrial myocyte ANP synthesis, which suggests a potential role for this hormone in overriding mineralocorticoid-induced renal sodium retention.
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