In the guinea-pig renal pelvis, most smooth muscle cells examined (>90%), u
sing a conventional microelectrode, had a resting membrane potential of abo
ut -50mV and produced spontaneous action potentials with initial fast spike
s and following plateau potentials. The remainder (<10%) had a resting memb
rane 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 aboli
shed by nifedipine, suggesting a possible contribution of voltage-gated Ca2
+ channels to the generation of these potentials. Niflumic acid and 4,4'-di
isothiocyanostilbene-2,2'-disulfonic acid (DIDS), inhibitors of Ca2+-activa
ted Cl- channels, showed different effects on the spontaneous action potent
ials, and the former but not the latter inhibited the activities, raised th
e question of an involvement of Cl- channels in the generation of these act
ivities. Depleting internal Ca2+ stores directly with caffeine or indirectl
y by inhibiting Ca2+-ATPase at the internal membrane with cyclopiazonic aci
d (CPA) prevented the generation of spontaneous activity. Chelating intrace
llular Ca2+ by 1,2-bis(2-aminophenoxy)ethane-N,N,N ',N'-tetraacetic acid (B
APTA) increased the amplitude of the spike component of spontaneous activit
y. Indomethacin inhibited the spontaneous activity, whereas prostaglandin F
-2<alpha> enhanced it. The results indicate that in smooth muscle of the re
nal pelvis, the generation of spontaneous activity is causally related to t
he activation of voltage-gated Ca2+ channels through which the influx of Ca
2+ may trigger the release of Ca2+ from the internal stores to activate a s
et of ion channels at the membrane. Endogenous prostaglandins may be involv
ed in the initiation of spontaneous activity.