Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats
Raff, H.; Roarty, T.P.
American Journal of Physiology 254(3 Pt 2): R431-R435
1988
ISSN/ISBN: 0002-9513 PMID: 2831742 Document Number: 305879
The control of aldosterone secretion may be altered during acute changes in arterial blood cases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 .+-. 2.0 ng .cntdot. ml-1 .cntdot. h-1), ACTH (96 .+-. 32 pg/ml), and ALDO (10 .+-. 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 .+-. 69 pg/ml) and ALDO (to 33 .+-. 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 .+-. 14 pg/ml) and ALDO (to 30 .+-. 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 .+-. 2 ng .cntdot. ml-1 .cntdot. h-1), ACTH (to 3977 .+-. 1114 pg/ml), and ALDO (to 41 .+-. 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (< 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (PO2 .apprx. 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.