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Regulation of Aldosterone Secretion During Hypoxemia at Sea Level and Moderately High Altitude^*

Divisions of Nephrology, Pulmonary, and Critical Care, Department of Internal Medicine, James A. Haley Veterans Administration Hospital Tampa, Florida 33612
the Department of Physiology, University of South Florida College of Medicine Tampa, Florida 33612
the Pulmonary Division, Department of Internal Medicine, Dartmouth Medical School Hanover, New Hampshire 03755

Address all correspondence and requests for reprints to: German Ramirez, M.D. (111-F), James A. Haley Veterans Administration Hospital, 13000 Bruce B. Downs Boulevard, Tampa, Florida 33612.

The aldosterone and cortisol responses to small doses of ACTH (0.125, 0.25, 0.5, and 1.25 µg) after dexamethasone administration were measured in normal subjects at sea level while breathing room air (mean O₂ saturation, 97 ± 0.9%) and again while breathing hypoxic gas to lower the O₂ saturation to 90%. A population of subjects matched for age and sex adapted to 3000 meters above sea level living in Colombia, South America, was also studied (mean O₂ saturation, 94 ± 0.7%). Hypoxemia, either induced at sea level or as a consequence of high altitude living, resulted in significant inhibition of aldosterone secretion after progressive administration of increasing doses of ACTH, but did not affect the cortisol response to ACTH. In addition, it was associated with higher plasma atrial natriuretic hormone levels. PRA declined only during acute hypoxemia induced at sea level and did not change during sea level normoxemia or high altitude living. Plasma sodium and potassium concentrations were no different in the three experimental conditions. We conclude that hypoxemia inhibits ACTH-stimulated aldosterone secretion and speculate that atrial natriuretic hormone may have mediated this effect.

^* This work was supported in part by Grant HL-37235 from the NIH, the Renal Research and Education Fund, the University of South Florida, and the James A. Haley V.A. Hospital.

Received April 14, 1988.

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