Atrial natriuretic factor inhibits Ca (2+) -dependent K+ fluxes in cultured vascular smooth muscle cells
Garay, R.; Hannaert, P.; Rodrigue, F.; Dunham, B.; Marche, P.; Genest, J.; Braquet, P.; Bianchi, C.; Cantin, M.; Meyer, P.
Journal of Hypertension. Suppl Official Journal of the International Society of Hypertension 3(3): S297-S298
1985
ISSN/ISBN: 0952-1178 PMID: 2856721 Document Number: 262160
The interaction of the synthetic fragment Arg101-Tyr126 of atrial natriuretic factor (ANF) with Ca(2+)-dependent K+ efflux was studied in the following six different cell models: cultured vascular smooth muscle cells from rat aorta; isolated rat glomeruli; human platelets; cultured endothelial cells from bovine aorta; peritoneal mouse macrophages; human red cells. In human red cells and mouse macrophages, the dose-response curves of K+ efflux as a function of Ca2+ ionophore, A23187, concentration were not modified by addition of ANF. In endothelial cells and platelets, ANF slightly inhibited Ca(2+)-dependent K+ efflux. In renal glomeruli, ANF inhibits about one-third of this flux and in vascular smooth muscle cells ANF induced a five- to tenfold increase in the EC50 of A23187 effect. In experiments performed at constant concentrations of A23187, the IC50 of ANF was approximately 10(-9) mol/l. Similar results were obtained in mouse macrophages with cyclic GMP (cGMP). Our results suggest that ANF is able to counterbalance an increase in cytosolic free Ca2+ content in vascular smooth muscle and some glomerular cells. This effect may result from the ability of this hormone to stimulate cGMP synthesis.