title: Somatostatin and insulin secretion from pancreatic islets: studies on the effect of high K+, 9-aminoacridine and valinomycin.
abstract: We attempted to determine whether a decrease in the potassium permeability of the D cell membrane plays a role in the stimulus-secretion coupling, as it does in the pancreatic B cell. Elevation in the extracellular potassium concentration from 5.5 to 16.5 mM, or 0.2 mM 9-aminoacridine, which decreases potassium permeability in plasma membrane, stimulated the release of somatostatin as well as insulin from the isolated rat pancreatic islets. Valinomycin (1 microM), a potassium ionophore inhibited the secretion in response to high glucose, high extracellular potassium or 9-aminoacridine. These findings indicate that a reduction in potassium permeability in the D cell membrane, as induced by glucose or other stimulants, may be a major step in secretion of somatostatin.
mesh_terms: D000585:Aminacrine / Q000494:pharmacology*; D000609:Aminoacridines / Q000494:pharmacology*; D000818:Animals; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013004:Somatostatin / Q000378:metabolism*; D014634:Valinomycin / Q000494:pharmacology*
chemical_list: D000609:Aminoacridines; D007328:Insulin; D014634:Valinomycin; D013004:Somatostatin; D000585:Aminacrine; D011188:Potassium