Role of K+ channels in maintaining the synchrony of spontaneous Ca2+ transients in the mural cells of rat rectal submucosal arterioles.

摘要: Mural cells in precapillary arterioles (PCAs) generate spontaneous Ca2+ transients primarily arising from the periodic release of sarcoendoplasmic reticulum (SR/ER). The induces Ca2+-activated chloride channel (CaCC)-dependent depolarisations that spread to neighbouring mural develop synchrony their transients. Here, we explored roles K+ channels maintaining Intracellular dynamics were visualised by Cal-520 fluorescence imaging submucosal PCAs rat rectum. Increasing extracellular concentration ([K+]o) 5.9 29.7 mM converted synchronous into asynchronous, high-frequency Similarly, blockade inward rectifier (Kir) with Ba2+ (50 μM) or Kv7 voltage-dependent (Kv7) XE 991 (10 μM) disrupted transients, while blockers for large-, intermediate- small-conductance had no effect. Kir2.1 immunoreactivity was detected arteriolar endothelium but not cells. In been pretreated Ba2+, nifedipine (1 μM) attenuated asynchronous failed restore synchrony. contrast, levcromakalim, an ATP-sensitive opener, restored Thus, constitutively active and Kir appear be involved relatively hyperpolarised membrane prevents depolarisation-induced ‘premature’ ensure sufficient SR/ER refilling is required regenerative resulting amongst