title: Functional and morphological properties of pericytes in suburothelial venules of the mouse bladder.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cell Physiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan. hasitani@med.nagoya-cu.ac.jp
authors.forename: Hikaru
authors.initials: H
authors.lastname: Hashitani
authors.forename: Retsu
authors.initials: R
authors.lastname: Mitsui
authors.forename: Yuki
authors.initials: Y
authors.lastname: Shimizu
authors.forename: Ryuhei
authors.initials: R
authors.lastname: Higashi
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Nakamura
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology*; D002478:Cells, Cultured; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D020286:Pericytes / Q000502:physiology* / Q000648:ultrastructure; D011817:Rabbits; D014521:Urethra / Q000166:cytology; D001743:Urinary Bladder / Q000098:blood supply / Q000187:drug effects / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D014699:Venules / Q000166:cytology* / Q000502:physiology
chemical_list: D002118:Calcium