1. Peristalsis in the smooth muscle cell (SMC) wall of the pyeloureteric system is unique in physiology in that the primary pacemaker resides in a population of atypical SMCs situated near the border of the renal papilla. 2. Atypical SMCs display high frequency Ca(2+) transients upon the spontaneous release of Ca(2+) from IP(3)-dependent stores that trigger cation-selective spontaneous transient depolarizations (STDs). In nifedipine, these Ca(2+) transients and STDS seldom propagate >100 mum. Synchronization of STDs in neighbouring atypical SMCs into an electrical signal that can trigger action potential discharge and contraction in the typical SMC layer involves a coupled oscillator mechanism dependent on Ca(2+) entry through L-type voltage-operated Ca(2+) channels. 3. A population of spindle- or stellate-shaped cells, immuno-positive for the tyrosine receptor kinase kit, are sparsely distributed throughout the pyeloureteric system. Ca(2+) transients and action potentials of long duration occurring at low frequencies are also recorded in a population of fusiform cells, which we have termed interstitial cells of Cajal-like cells (ICC-like cells). 4. The electrical and Ca(2+) signals in ICC-like cells are abolished upon blockade of Ca(2+) release from either IP(3)- or ryanodine-dependent Ca(2+) stores. However, the spontaneous Ca(2+) signals in atypical SMCs or ICC-like cells are little affected in W/W(-v) transgenic mice which have extensive lesions of their intestinal ICC networks. 5. In summary, we have developed a model of pyeloureteric pacemaking in which atypical SMCs are indeed the primary pacemakers, the function of ICC-like cells has yet to be determined.
|Pages (from-to)||509 - 515|
|Number of pages||7|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 2010|