MODULATION OF CA2-ACTIVATED K+ CHANNELS IN HUMAN VASCULAR CELLS BY INSULIN AND BASIC FIBROBLAST-GROWTH-FACTOR()

Insulin and basic fibroblast growth factor (bFGF) play an important ro le in the pathogenesis of atherosclerosis and have been shown to have vasodilatory effects. Since modulation of vascular ion channels determ ines membrane potential and thereby influences essential Ca2+-dependen t intracellular pathways, we have investigated the effect of insulin a nd bFGF on Ca2+-activated K+ channels (BKCa) in human umbilical vein e ndothelial cells (HUVEC) and smooth muscle cells. The latter were obta ined from either atherosclerotic plaques (SMCP) or from media segments (SMCM) of human coronary arteries. Using the patch-clamp technique, i nsulin (100 mu U/ml) caused a significant increase in BKCa open-state probability in SMCP and HUVEC, whereas no significant changes were obs erved in SMCM. Basic FGF (30 ng/ml) revealed a significant increase in BKCa activity in HUVEC and a significant decrease in the BKCa open-st ate probability in SMCP, but caused no changes in SMCM. Thus, growth f actors modulate vascular BKCa in a cell-type specific manner, which ma y be of importance concerning vasoactive and atherogenic effects of gr owth factors. (C) 1998 Churchill Livingstone