Functional and morphological properties of pericytes in suburothelial venules of the mouse bladder

Background and Purpose In suburothelial venules of rat bladder, pericytes (perivascular cells) develop spontaneous Ca2+ transients, which may drive the smooth muscle wall to generate spontaneous venular constrictions. We aimed to further explore the morphological and functional characteristics of pericytes in the mouse bladder. Experimental Approach The morphological features of pericytes were investigated by electron microscopy and fluorescence immunohistochemistry. Changes in diameters of suburothelial venules were measured using video microscopy, while intracellular Ca2+ dynamics were visualized using Fluo-4 fluorescence Ca2+ imaging. Key Results A network of a-smooth muscle actin immunoreactive pericytes surrounded venules in the mouse bladder suburothelium. Scanning electron microscopy revealed that this network of stellate-shaped pericytes covered the venules, while transmission electron microscopy demonstrated that the venular wall consisted of endothelium and adjacent pericytes, lacking an intermediate smooth muscle layer. Pericytes exhibited spontaneous Ca2+ transients, which were accompanied by phasic venular constrictions. Nicardipine (1?mu M) disrupted the synchrony of spontaneous Ca2+ transients in pericytes and reduced their associated constrictions. Residual asynchronous Ca2+ transients were suppressed by cyclopiazonic acid (10?mu M), 2-aminoethoxydiphenyl borate (10?mu M), U-73122 (1?mu M), oligomycin (1?mu M) and SKF96365 (10?mu M), but unaffected by ryanodine (100?mu M) or YM-244769 (1?mu M), suggesting that pericyte Ca2+ transients rely on Ca2+ release from the endoplasmic reticulum via the InsP3 receptor and also require Ca2+ influx through store-operated Ca2+ channels. Conclusions and Implications The pericytes in mouse bladder can generate spontaneous Ca2+ transients and contractions, and thus have a fundamental role in promoting spontaneous constrictions of suburothelial venules.