Properties of spontaneous electrical activity in smooth muscle of the guinea-pig renal pelvis

In the guinea-pig renal pelvis, most smooth muscle cells examined (>90%), using a conventional microelectrode, had a resting membrane potential of about -50mV and produced spontaneous action potentials with initial fast spikes and following plateau potentials. The remainder (<10%) had a resting membrane potential of about -40 mV and produced periodical depolarization with slow rising and falling phases. Experiments were carried out to investigate the properties of spontaneous action potentials. The potentials were abolished by nifedipine, suggesting a possible contribution of voltage-gated Ca2+ channels to the generation of these potentials. Niflumic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), inhibitors of Ca2+-activated Cl- channels, showed different effects on the spontaneous action potentials, and the former but not the latter inhibited the activities, raised the question of an involvement of Cl- channels in the generation of these activities. Depleting internal Ca2+ stores directly with caffeine or indirectly by inhibiting Ca2+-ATPase at the internal membrane with cyclopiazonic acid (CPA) prevented the generation of spontaneous activity. Chelating intracellular Ca2+ by 1,2-bis(2-aminophenoxy)ethane-N,N,N ',N'-tetraacetic acid (BAPTA) increased the amplitude of the spike component of spontaneous activity. Indomethacin inhibited the spontaneous activity, whereas prostaglandin F-2<alpha> enhanced it. The results indicate that in smooth muscle of the renal pelvis, the generation of spontaneous activity is causally related to the activation of voltage-gated Ca2+ channels through which the influx of Ca2+ may trigger the release of Ca2+ from the internal stores to activate a set of ion channels at the membrane. Endogenous prostaglandins may be involved in the initiation of spontaneous activity.