title: Role of Ca2+ entry and Ca2+ stores in atypical smooth muscle cell autorhythmicity in the mouse renal pelvis.
abstract: OBJECTIVE
  Electrically active atypical smooth muscle cells (ASMCs) within the renal pelvis have long been considered to act as pacemaker cells driving pelviureteric peristalsis. We have investigated the role of Ca2+ entry and uptake into and release from internal stores in the generation of Ca2+ transients and spontaneous transient depolarizations (STDs) in ASMCs.
  
  
  METHODS
  The electrical activity and separately visualized changes in intracellular Ca2+ concentration in typical smooth muscle cells (TSMCs), ASMCs and interstitial cells of Cajal-like cells (ICC-LCs) were recorded using intracellular microelectrodes and a fluorescent Ca2+ indicator, fluo-4.
  
  
  RESULTS
  In 1 microM nifedipine, high frequency (10-30 min(-1)) Ca2+ transients and STDs were recorded in ASMCs, while ICC-LCs displayed low frequency (1-3 min(-1)) Ca2+ transients. All spontaneous electrical activity and Ca2+ transients were blocked upon removal of Ca2+ from the bathing solution, blockade of Ca2+ store uptake with cyclopiazonic acid (CPA) and with 2-aminoethoxy-diphenylborate (2-APB). STD amplitudes were reduced upon removal of the extracellular Na+ or blockade of IP3 dependent Ca2+ store release with neomycin or U73122. Blockade of ryanodine-sensitive Ca2+ release blocked ICC-LC Ca2+ transients but only reduced Ca2+ transient discharge in ASMCs. STDs in ASMCS were also little affected by DIDS, La3+, Gd3+ or by the replacement of extracellular Cl(-) with isethionate.
  
  
  CONCLUSIONS
  ASMCs generated Ca2+ transients and cation-selective STDs via mechanisms involving Ca2+ release from IP3-dependent Ca2+ stores, STD stimulation of TSMCs was supported by Ca2+ entry through L type Ca2+ channels and Ca2+ release from ryanodine-sensitive stores.
authors.affiliation: Department of Physiology, School of Biomedical Sciences, Monash University, Clayton, Victoria, Australia. rick.lang@med.monash.edu.au
authors.forename: R J
authors.initials: RJ
authors.lastname: Lang
authors.forename: H
authors.initials: H
authors.lastname: Hashitani
authors.forename: M A
authors.initials: MA
authors.lastname: Tonta
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: H C
authors.initials: HC
authors.lastname: Parkington
mesh_terms: D000818:Animals; D001896:Boron Compounds / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000378:metabolism*; D004594:Electrophysiology; D007211:Indoles / Q000494:pharmacology; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D007682:Kidney Pelvis; D008297:Male; D051379:Mice; D009119:Muscle Contraction / Q000502:physiology*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D009543:Nifedipine / Q000494:pharmacology; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
chemical_list: D001896:Boron Compounds; D020746:Calcium Channels, L-Type; D007211:Indoles; D019837:Ryanodine Receptor Calcium Release Channel; D015544:Inositol 1,4,5-Trisphosphate; D012964:Sodium; C109986:2-aminoethoxydiphenyl borate; D009543:Nifedipine; D002118:Calcium; C000543:cyclopiazonic acid