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

Citation
H. Takano et al., Properties of spontaneous electrical activity in smooth muscle of the guinea-pig renal pelvis, JPN J PHYSL, 50(6), 2000, pp. 597-603
Citations number
28
Categorie Soggetti
Physiology
Journal title
JAPANESE JOURNAL OF PHYSIOLOGY
ISSN journal
0021521X → ACNP
Volume
50
Issue
6
Year of publication
2000
Pages
597 - 603
Database
ISI
SICI code
0021-521X(200012)50:6<597:POSEAI>2.0.ZU;2-3
Abstract
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.