title: Effects of hypoxia and atrial natriuretic peptide on aldosterone secretion in healthy subjects.
abstract: To evaluate the inhibitory effect of hypoxia and atrial natriuretic peptide (ANP) on aldosterone secretion, 11 healthy male subjects were infused with 5 ng.kg-1 x min-1 ANP or placebo. The subjects were exposed in a stepwise fashion to incremental hypobaric hypoxia, which decreased arterial oxygen saturation to 79 +/- 2% in the placebo and 84 +/- 2% in the ANP condition (P < 0.05). In the placebo condition, the plasma ANP concentration increased from 13.8 +/- 1.0 to 19.6 +/- 2.3 pmol/l (P < 0.01) at the lowest barometric pressure. Plasma renin activity did not change, whereas the plasma aldosterone levels increased consequent to the increase of plasma adrenocorticotropic hormone (ACTH). Continuous infusion of ANP increased the plasma levels twofold (P < 0.001) and the level of guanosine 3',5'-cyclic monophosphate threefold (P < 0.001). However, the plasma aldosterone concentrations were not different in the two experimental conditions. Administration of supplementary oxygen significantly decreased ACTH to baseline values (P < 0.01) together with a decrease in aldosterone. Free water clearance (P = 0.05) but not sodium excretion (P = NS) increased during continuous ANP infusion. The data indicate that the aldosterone secretion in hypoxia is not inhibited by (patho)physiological plasma ANP levels. The inhibition of aldosterone secretion may well be explained by a direct effect of hypoxia on the adrenal cells. ACTH is a major stimulus of aldosterone secretion in hypoxia, which overrides the natriuretic effect of ANP.
authors.affiliation: Department of General Internal Medicine, University Hospital Leiden, The Netherlands.
authors.forename: R G
authors.initials: RG
authors.lastname: Westendorp
authors.forename: A N
authors.initials: AN
authors.lastname: Roos
authors.forename: M
authors.initials: M
authors.lastname: Simons
authors.forename: W
authors.initials: W
authors.lastname: Wertheim
authors.forename: F H
authors.initials: FH
authors.lastname: Bosch
authors.forename: M
authors.initials: M
authors.lastname: Frölich
authors.forename: A E
authors.initials: AE
authors.lastname: Meinders
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000450:Aldosterone / Q000097:blood*; D001274:Atmospheric Pressure; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000494:pharmacology*; D001810:Blood Volume / Q000502:physiology; D002245:Carbon Dioxide / Q000097:blood; D006152:Cyclic GMP / Q000097:blood / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism*; D007457:Iodine Radioisotopes; D008297:Male; D010100:Oxygen / Q000097:blood; D012083:Renin / Q000097:blood; D016037:Single-Blind Method; D012964:Sodium / Q000378:metabolism
chemical_list: D007457:Iodine Radioisotopes; D002245:Carbon Dioxide; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D012083:Renin; D006152:Cyclic GMP; D010100:Oxygen; D006854:Hydrocortisone