Synchrony of spontaneous Ca2+ activity in microvascular mural cells.

摘要: Spontaneous rhythmic constrictions known as vasomotion are developed in several microvascular beds vivo. Vasomotion arterioles is considered to facilitate blood flow, while venular would tissue metabolite drainage. Mechanisms underlying periodically generate synchronous Ca2+ transients vascular smooth muscle cells (VSMCs). In visceral organs, mural (pericytes and VSMCs) arterioles, capillaries venules exhibit spontaneous transients. Since sympathetic regulation rather limited the intra-organ microvessels, activity of may play an essential role maintaining perfusion. Synchronous precapillary (PCAs)/capillaries appear propagate upstream drive their vasomotion, develop own associated vasomotion. primarily arise from IP3 and/or ryanodine receptor-mediated release sarcoendoplasmic reticulum (SR/ER) stores. The resultant opening Ca2+-activated Cl- channels (CaCCs) causes a membrane depolarisation that triggers influx via T-type L-type voltage-dependent (VDCCs). Mural electrically coupled with each other gap junctions, thus allow sequential spread CaCC or VDCC-dependent depolarisations synchrony within network. Importantly, also requires certain range resting potential maintained by Kv7 K+ (Kv7) inward rectifier (Kir) channels. Thus, depolarised evoke asynchronous, 'premature' transients, hyperpolarised prevents any activity.