Investigation of the relationship between cell-surface calcium-ion gating and phosphatidylinositol turnover by comparison of the effects of elevated extracellular potassium ion concentration on ileium smooth muscle and pancreas

Abstract

Incubation of fragments of guinea pig ileum smooth muscle in the presence of an elevated extracellular K+ concentration, which caused an increase in cell-surface Ca2+ premeability and led to contraction, caused a marked increase in phosphatidylinositol turnover, as assessed by incorporation of 32Pi. This response was not diminished by atropine or propylbenzilylcholine mustard, 2 muscarinic cholinergic antagonists, and was not caused by the release of endogenous acetylcholine within the tissue. In contrast, exposure of guinea pig pancreas fragments to high extracellular [K+], which does not increase cell-surface Ca2+ permeability or evoke secretion, did not increase phosphatidylinositol turnover, even though such an increase was triggered by carbamoylcholine, which was a secretagogue. The suggested function for phosphatidylinositol breakdown in the mechanisms of cell-surface Ca2+ gates was supported.