Alpha-adrenergic regulation of cellular functions and cAMP

Abstract

Rat islets, rat intestinal epithelium and mouse thyroid were used as models for the studies of alpha-adrenergic regulation of cellular functions and cAMP. (1) Insulin release from the islets and cAMP content were inhibited by alpha2 stimulation. However, alpha2 stimulation also inhibited the Bt2cAMP-induced insulin release. Therefore, it appears that the inhibition of insulin release by alpha2 stimulation could not be explained solely by the inhibition of adenylate cyclase activity. (2) Cholera toxin, prostaglandin E1, or Bt2CAMP elicited intestinal secretion in the jejunum. All the secretions above were inhibited by alpha2 stimulation. 3H-Yohimbine binding revealed the presence of alpha2 receptors in the small intestinal epithelium. However, alpha2 stimulation failed to reduce cAMP content in these cells. (3) Alpha1 stimulation inhibited thyroxine release without reducing cAMP levels, but stimulated phosphatidylinositol (PI) turnover. However, TSH, which stimulated thyroxine release, also enhanced PI turnover. Therefore, it appears that alphai-adrenergic inhibition of thyroxine release could not be explained by the enhancement of PI turnover. The results suggest that islet alpha2 receptors are involved in some unknown mechanism besides adenylate cyclase inhibition and that mouse thyroid alphai and rat intestinal epithelium alpha2 receptors are involved in some mechanisms other than inhibition of the cyclase activity.