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This Article Full Text Full Text (PDF) All Versions of this Article: 583/3/1049    most recent jphysiol.2007.137034v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lang, R. J. Articles by Suzuki, H. Search for Related Content PubMed PubMed Citation Articles by Lang, R. J. Articles by Suzuki, H. Related Collections Renal and Endocrine

¹ Department of Physiology, School of Biomedical Sciences, Faculty of Medicine and Health Sciences, Monash University, Clayton, Victoria 3800, Australia
² Department of Regulatory Cell Physiology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan

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 Ca²⁺ concentration in typical smooth muscle cells (TSMCs), ASMCs and ICC-LCs using intracellular microelectrodes and a fluorescent Ca²⁺ indicator, fluo-4. Nifedipine (1–10 µM)-sensitive driven action potentials and Ca²⁺ 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) Ca²⁺ transients and spontaneous transient depolarizations (STDs) were recorded in ASMCs in the absence or presence of 1 µM nifedipine. ICC-LCs displayed low frequency (1–3 min^–1) Ca²⁺ transients which we speculated arose from cells that displayed action potentials with long plateaus (2–5 s). Neither electrical activity propagated over distances > 50 µm. In 1 µM nifedipine, ASMCs or ICC-LCs separated by < 30 µm displayed some synchronicity in their Ca²⁺ 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.

(Received 21 May 2007; accepted after revision 24 July 2007; first published online 26 July 2007)
Corresponding author R. J. Lang: Department of Physiology, Monash University, Clayton, Victoria 3800, Australia. Email: rick.lang{at}med.monash.edu.au

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