Vascular endothelial cells control the vasomotor responses in two mechanisms. An agonist stimulation applied to the endothelium increases the endothelial intracellular concentration of Ca2+, which triggers a release of vasoactive substances such as NO and PGI2. These substances diffuse to the smooth muscle cells and modulate their mechanical activities by the pharmacomechanical coupling. Increased endothelial intracellular Ca2+ also activates the Ca2+-activated K+ channels quickly and the Ca2+-activated non-selective cation channels gradually evoking endothelial hyperpolarization and depolarization, respectively. These changes in endothelial membrane potential conduct to the smooth muscle cells via the myoendothelial gap junctions and the contraction of the smooth muscle cells is modulated by the electromechanical coupling. As the electromechanical mechanism is most effective in arterioles which have only one or two layers of smooth muscle cells, this mechanism seems to be crucial in controlling the total peripheral resistance that is mainly determined by this portion of vasculature.
雑誌名
名古屋市立大学看護学部紀要
雑誌名(英)
Bulletin of Nagoya City University School of Nursing