Carbachol has opposite effects to glucose in raising the sodium content of pancreatic islets.

Integrating flame photometry was used for measuring sodium in single pancreatic islets from ob/ob mice. Exposure to 100 microM carbachol resulted in a 25-40% increase in sodium without any effect on potassium during incubation with 0-5 mM glucose in media deficient or not in Ca2+. This action of carbachol was abolished by 10 microM atropine or by raising the glucose concentration to 20 mM. A minor increase of the steady state content of sodium occurred in the presence of 200 microM ATP or 10 nM tetradecanoylphorbol 13-acetate (TPA). Carbachol differed from TPA in markedly stimulating sodium accumulation after ouabain inhibition of the Na/K pump. The results indicate that muscarinic receptor activation has opposite effects to glucose in inducing a rise of the islet content of sodium. It is suggested that the cholinergic control of the endocrine pancreas involves entry of Na+ in addition to the Na+ entry mediated by protein kinase C activation of Na+/H+ countertransport.