Glucoregulatory role of cortisol and epinephrine interactions studied in adrenalectomized dogs.

Abstract

The importance of basal cortisol (H) and epinephrine (E) levels on glucoregulation, and the effects of E, given to simulate moderate to severe stress (5 times basal rate of infusion), were examined in seven conscious adrenalectomized dogs. Although plasma glucagon (IRG) increased by 47%, insulin (IRI) decreased by 36%, norepinephrine (NE) increased by 103%, and FFA decreased by 26%, glucose concentration and kinetics remained normal after adrenalectomy. A 4-h infusion of H reestablished basal cortisol levels and returned IRG to its basal preadrenalectomy level with no change in IRI, NE, and FFA levels. Glucose production and metabolic clearance decreased concomitantly by 20%, maintaining euglycemia. A 90-min infusion of basal E caused only a transient increase in IRG. The simultaneous infusion of H with E prevented this increase in IRG and returned IRI to preadrenalectomy levels in the absence of any change in NE or glucose. A subsequent infusion of five times basal E, alone, raised circulating E levels and caused a transient decrease in plasma NE, but no change in IRI. There was a similar hyperglycemic response, as seen previously in normal dogs. The simultaneous infusion of H and E prevented the decrease in NE, but did not change the IRI and FFA responses. There was an 80% greater plasma glucose response than seen during infusion of E alone. In conclusion, what E and H lack after adrenalectomy is compensated for by an increase in IRG and a decrease in IRI, and normal glucose concentrations and kinetics are maintained. It appeared that normoglucagonemia required basal H release, whereas normoinsulinemia required both basal H and E secretion.(ABSTRACT TRUNCATED AT 250 WORDS)