VASOMOTOR-ACTIVE FACTORS DERIVED FROM ENDOTHELIALCELLS IN MICE ARTERIES.

There is enough evidence indicating that biologically active substances released from the endothelial cells of blood vessels play physiologically and/or pathophysiologically important roles in regulating thrombogenesis or development of atherosclerosis。Especially，balance of endothelium-derived constricting factors(EDCF)and endothelium-derived relaxing factors(EDRF)is very important。We found that EDHF(endothelium-derived hyperpolarizing faetor)，one of EDRF，regulates actively vasomotor tone of smaller arteries less than 300 mm in diameter in rats，and hyperpolarization which EDHF produces in arterial smooth muscle cells by activating apamin-and charibdotoxin-sensitive K Ii D1+D1channels decreases Ca Ii D12+it D1sensitivity of contractile elements as well inbiting decreases decreases Ca D12+decreases Caitivity of contractile elements as well biting decreases decreases Ca D12+decreases.We also found that EDHF plays an essential role in maintaining endothelial function regulating vasomotor tone of arteries as a backup system to EDNO in female rats.In order to clarify more the physiological or pathophysiological significance of EDHF and its molecular mechanism，more sophisticated studies such as those using transgenic mice are required in near future.We found that Microvessel Perfusion System is adequate experimental methods observing changes in vasomotor tone of very small arteries obtained from small animals such as mice.

There is enough evidence indicating that biologically active substances released from the endothelial cells of blood vessels play physiologically and/or pathophysiologically important roles in regulating thrombogenesis or development of atherosclerosis. Especially, balance of endothelium-derived constricting factors(EDCF) and endothelium-derived relaxing factors(EDRF) is very important. We found that EDHF(endothelium-derived hyperpolarizing faetor) , one of EDRF, regulates actively vasomotor tone of smaller arteries less than 300 mm in diameter in rats, and hyperpolarization which EDHF produces in arterial smooth muscle cells by activating apamin-and charibdotoxin-sensitive KィイD1+ィエD1 channels decreases CaィイD12+ィエD1 sensitivity of contractile elements as well as inhibiting CaィイD12+ィエD1 influx through L-type CaィイD12+ィエD1 channels. We also found that EDHF plays an essential role in maintaining endothelial function regulating vasomotor tone of arteries as a backup system to EDNO in female rats. In order to clarify more the physiological or pathophysiological significance of EDHF and its molecular mechanism, more sophisticated studies such as those using transgenic mice are required in near future. We found that Microvessel Perfusion System is adequate experimental methods observing changes in vasomotor tone of very small arteries obtained from small animals such as mice.