Adrenergic control of somatostatin release.
The effects of adrenergic stimulation and suppression on somatostatin (SS), insulin, and glucagon release were studied in intact dogs. Isoproterenol, a beta-adrenergic agonist, significantly increased portal venous and arterial levels of SS and arterial levels of insulin and glucagon. Propranolol, a beta-adrenergic antagonist, significantly decreased portal venous SS and suppressed the isoproterenol-stimulated increases in the levels of SS, insulin, and glucagon. alpha-Adrenergic stimulation (propranolol plus epinephrine) decreased portal venous SS and arterial insulin. Phentolamine, and alpha-adrenergic antagonist, increased portal venous and arterial SS and arterial glucagon. These data suggest that in intact dogs, stimulation of beta-adrenergic receptors enhances the release of SS, insulin, and glucagon, while stimulation of alpha-adrenergic receptors inhibits the release of SS and insulin without having a definitive effect on glucagon.
D000818:Animals; D004285:Dogs; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D005934:Glucagon / Q000097:blood; D007328:Insulin / Q000097:blood; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D010646:Phentolamine / Q000494:pharmacology; D011169:Portal Vein; D011433:Propranolol / Q000494:pharmacology; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000502:physiology*; D013004:Somatostatin / Q000097:blood*
D007328:Insulin; D011941:Receptors, Adrenergic; D013004:Somatostatin; D005934:Glucagon; D011433:Propranolol; D007545:Isoproterenol; D004837:Epinephrine; D010646:Phentolamine