Spontaneous electrical and Ca2+ signals in typical and atypical smooth muscle cells and interstitial cell of Cajal-like cells of mouse renal pelvis.
Electrical rhythmicity in the renal pelvis provides the fundamental drive for the peristaltic contractions that propel urine from the kidney to bladder for storage until micturition. Although atypical smooth muscles (ASMCs) within the most proximal regions of the renal pelvis have long been implicated as the pacemaker cells, the presence of a sparsely distributed population of rhythmically active Kit-positive interstitial cells of Cajal-like cells (ICC-LCs) have confounded our understanding of pelviureteric peristalsis. We have recorded the electrical activity and separately visualized changes in intracellular Ca(2+) concentration in typical smooth muscle cells (TSMCs), ASMCs and ICC-LCs using intracellular microelectrodes and a fluorescent Ca(2+) indicator, fluo-4. Nifedipine (1-10 microm)-sensitive driven action potentials and Ca(2+) waves (frequency 6-15 min(-1)) propagated through the TSMC layer at a velocity of 1-2 mm s(-1). High frequency (10-40 min(-1)) Ca(2+) transients and spontaneous transient depolarizations (STDs) were recorded in ASMCs in the absence or presence of 1 microm nifedipine. ICC-LCs displayed low frequency (1-3 min(-1)) Ca(2+) transients which we speculated arose from cells that displayed action potentials with long plateaus (2-5 s). Neither electrical activity propagated over distances > 50 microm. In 1 microm nifedipine, ASMCs or ICC-LCs separated by < 30 microm displayed some synchronicity in their Ca(2+) transient discharge suggesting that they may well be acting as 'point sources' of excitation to the TSMC layer. We speculate that ASMCs act as the primary pacemaker in the renal pelvis while ICC-LCs play a supportive role, but can take over pacemaking in the absence of the proximal pacemaker drive.
Lang
Richard J
RJ
Department of Physiology, School of Biomedical Sciences, Faculty of Medicine and Health Sciences, Monash University, Clayton, Victoria 3800, Australia. rick.lang@med.monash.edu.au
Hashitani
Hikaru
H
Tonta
Mary A
MA
Parkington
Helena C
HC
Suzuki
Hikaru
H
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D017629:Gap Junctions / Q000187:drug effects / Q000502:physiology; D006034:Glycyrrhetinic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D066298:In Vitro Techniques; D007682:Kidney Pelvis / Q000166:cytology / Q000502:physiology*; D008297:Male; D051379:Mice; D008839:Microelectrodes; D009119:Muscle Contraction / Q000502:physiology; D009130:Muscle, Smooth / Q000166:cytology / Q000502:physiology*; D032389:Myocytes, Smooth Muscle / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D010528:Peristalsis / Q000502:physiology*; D014513:Ureter / Q000502:physiology
D002121:Calcium Channel Blockers; C119129:18alpha-glycyrrhetinic acid; D009543:Nifedipine; D006034:Glycyrrhetinic Acid; D002118:Calcium