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Low oxygen selectively inhibits aldosterone secretion from bovine adrenocortical cells in vitro

256 (Endocrinol. Metab. 19): E640-E644,1989.-Systemic hypoxia has been reported to inhibit selectively aldosterone secretion in vivo. The mechanismof this inhibition hasnot been elucidated.We hypothesized that decreased tissue POT directly inhibited aldosteronogenesis. test this hypothesis, we exTo posed dispersedadrenocortical cells (90% glomerulosa/lO% fasciculata) to decreasedPaz while simultaneously stimulating aldosteronesecretionwith angiotensinII, V,2’-Odibutyryladenosine 3’,5’-cyclic monophosphate (dibutyryl CAMP) adrenocorticotropic hormone (ACTH)-( l-24), or progesterone.Decreasingbuffer POT from ~150 to ~85 Torr significantly inhibited basaland angiotensinII, CAMP, progesterone, and ACTH-stimulated aldosteronesecretion at all doses of secretagogue. Inhibition waslargest for angiotensin II (55 $9% inhibition at 1 PM) and CAMP (54 t 8% at 3 mM) and lowest for ACTH (24% at 100 nM) and basal aldosterone secretion (31 k 7%). This inhibition was reversedby returning the buffer Paz to 150 Torr. Cortisol secretion was not significantly inhibited by decreasedbuffer POT. We conclude that decreased buffer Pop significantly inhibits aldosterone secretion , and this inhibition is reversible and specific. METHODS Hypoxia-induced inhibition of aldosterone secretion in vivo Reagents. The following materials were obtained from may be caused,at least in part, by a direct effect of low tissue these sources: collagenase I (CZostridium histolyticum Pop within the adrenal cortex. collagenase; EC from Worthington Biochemical hypoxia; http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Endocrinology and Metabolism The American Physiological Society

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