Renin, ACTH, and adrenocortical function during hypoxia and hemorrhage in conscious rats.
We studied the effect of chronic hypoxia on the renin, adrenocorticotropin (ACTH), aldosterone, and corticosterone responses to acute hemorrhage in conscious male rats with chronic femoral arterial catheters. Rats were exposed to 21, 12.5, or 10% O2 (n = 7 per group). At 42 h of exposure, animals underwent a rapid 6 ml/kg hemorrhage. O2 at 12.5 and 10% led to significant hypoxemia (arterial PO2 = 52 +/- 1 and 43 +/- 1 Torr, respectively) and respiratory alkalosis. Significant increases in plasma sodium to 145 +/- 2 meq/l and decreases in plasma potassium to 3.53 +/- 0.12 meq/l were also observed during hypoxia. Hypoxia per se had no significant effect on blood pressure, plasma renin activity, ACTH, and corticosterone. O2 at 12.5% led to a significant reduction in aldosterone levels (0.9 +/- 0.8 ng/dl) compared with normoxia (4.2 +/- 0.9 ng/dl). The mean arterial pressure, plasma renin activity, and aldosterone responses to hemorrhage were unaltered by hypoxia. ACTH and corticosterone responses to hemorrhage were potentiated by exposure to 10% O2. We conclude that chronic exposure to severe hypoxia augments the pituitary-adrenal but not the renin-aldosterone response to hemorrhage.
D000302:Adrenal Cortex / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000450:Aldosterone / Q000097:blood; D000704:Analysis of Variance; D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure; D003345:Corticosterone / Q000097:blood; D004573:Electrolytes / Q000097:blood; D006470:Hemorrhage / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D051381:Rats; D012083:Renin / Q000097:blood*
D004573:Electrolytes; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D012083:Renin; D003345:Corticosterone