biostudies-literatureUnknown167(8)Hashitani H<h4>Background and purpose</h4>In suburothelial venules of rat bladder, pericytes (perivascular cells) develop spontaneous Ca(2+) 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.<h4>Experimental approach</h4>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 Ca(2+) dynamics were visualized using Fluo-4 fluorescence Ca(2+) imaging.<h4>Key results</h4>A network of α-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 Ca(2+) transients, which were accompanied by phasic venular constrictions. Nicardipine (1 μM) disrupted the synchrony of spontaneous Ca(2+) transients in pericytes and reduced their associated constrictions. Residual asynchronous Ca(2+) transients were suppressed by cyclopiazonic acid (10 μM), 2-aminoethoxydiphenyl borate (10 μM), U-73122 (1 μM), oligomycin (1 μM) and SKF96365 (10 μM), but unaffected by ryanodine (100 μM) or YM-244769 (1 μM), suggesting that pericyte Ca(2+) transients rely on Ca(2+) release from the endoplasmic reticulum via the InsP(3) receptor and also require Ca(2+) influx through store-operated Ca(2+) channels.<h4>Conclusions and implications</h4>The pericytes in mouse bladder can generate spontaneous Ca(2+) transients and contractions, and thus have a fundamental role in promoting spontaneous constrictions of suburothelial venules.British journal of pharmacology1723-36https://www.ebi.ac.uk/biostudies/studies/S-EPMC3525874biostudies-literatureFunctional and morphological properties of pericytes in suburothelial venules of the mouse bladder.PMC3525874Hashitani HNakamura KMitsui RHigashi RShimizu YfalseFunctional and morphological properties of pericytes in suburothelial venules of the mouse bladder.<h4>Background and purpose</h4>In suburothelial venules of rat bladder, pericytes (perivascular cells) develop spontaneous Ca(2+) 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.<h4>Experimental approach</h4>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 Ca(2+) dynamics were visualized using Fluo-4 fluorescence Ca(2+) imaging.<h4>Key results</h4>A network of α-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 Ca(2+) transients, which were accompanied by phasic venular constrictions. Nicardipine (1 μM) disrupted the synchrony of spontaneous Ca(2+) transients in pericytes and reduced their associated constrictions. Residual asynchronous Ca(2+) transients were suppressed by cyclopiazonic acid (10 μM), 2-aminoethoxydiphenyl borate (10 μM), U-73122 (1 μM), oligomycin (1 μM) and SKF96365 (10 μM), but unaffected by ryanodine (100 μM) or YM-244769 (1 μM), suggesting that pericyte Ca(2+) transients rely on Ca(2+) release from the endoplasmic reticulum via the InsP(3) receptor and also require Ca(2+) influx through store-operated Ca(2+) channels.<h4>Conclusions and implications</h4>The pericytes in mouse bladder can generate spontaneous Ca(2+) transients and contractions, and thus have a fundamental role in promoting spontaneous constrictions of suburothelial venules.2012-01-01T00:00:00Z2012 Dec2024-10-17T17:33:04.156Z2019-03-27T01:02:00ZS-EPMC35258742286214310.1111/j.1476-5381.2012.02125.x