Atrial natriuretic peptide transcription, secretion, and glomerular receptor activity during mineralocorticoid escape in the rat.
The 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.
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics / Q000502:physiology*; D003900:Desoxycorticosterone / Q000494:pharmacology*; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D007678:Kidney Glomerulus / Q000378:metabolism; D008297:Male; D011498:Protein Precursors / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D017461:Receptors, Atrial Natriuretic Factor; D011956:Receptors, Cell Surface / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D014158:Transcription, Genetic
D011498:Protein Precursors; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D003900:Desoxycorticosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium; D017461:Receptors, Atrial Natriuretic Factor