Properties of synchronous spontaneous Ca transients in the mural cells of rat rectal arterioles.

Synchrony of spontaneous Ca transients among venular mural cells (smooth muscle cells and pericytes) in visceral organs relies on the intercellular spread of L-type voltage-dependent Ca channel (LVDCC)-dependent depolarisations. However, the mechanisms underlying the synchrony of spontaneous Ca transients between arteriolar mural cells are less understood. The spontaneous intracellular Ca dynamics of arteriolar mural cells in the rat rectal submucosa were visualised by Cal-520 Ca imaging to analyse their synchrony. The mural cells in fine arterioles that had a rounded cell body with several extended processes developed spontaneous 'synchronous' Ca transients arising from Ca released from sarcoendoplasmic reticulum Ca stores. Gap junction blockers (3 μM carbenoxolone, 10 μM 18β-glycyrrhetinic acid), a Ca-activated Cl channel (CaCC) blocker (100 μM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid) or lowering extracellular Cl concentration (from 134.4 to 12.4 mM) disrupted the synchrony of Ca transients between arteriolar mural cells. Blockers of T-type voltage-dependent Ca channels (TVDCCs, 1 μM mibefradil or ML218) or LVDCCs (1 μM nifedipine) reduced the Ca transient frequency or their area under curve (AUC), respectively. However, neither TVDCC nor LVDCC blockers disrupted the synchrony of Ca transients among arteriolar mural cells. This is in contrast with rectal venules in which nifedipine disrupted the synchrony of spontaneous Ca transients. Thus, spontaneous transient depolarisations arising from the opening of CaCCs may effectively spread to neighbouring arteriolar mural cells via gap junctions to maintain the Ca transient synchrony. Activation of TVDCCs appears to accelerate spontaneous Ca transients, while LVDCCs predominantly contribute to the duration of Ca transients.