Fast Na+ and slow Ca2+ channels in single uterine muscle cells from pregnant rats.
Whole cell voltage-clamp method was applied to single smooth muscle cells freshly isolated from the longitudinal layer of 18-day pregnant rat uterus. Inward currents were isolated after outward currents were minimized by use of high Cs+ in the pipette solution and 4-aminopyridine (3 mM) in the bath solution. Depolarizing pulses, applied from a holding potential of -90 mV, evoked two types of inward current, fast and slow. The fast inward current decayed and disappeared within 30 ms and depended on extracellular Na+ concentration. This fast current was inhibited by tetrodotoxin (TTX) dose dependently (KD = 27 nM). These results suggest that the fast inward current was a TTX-sensitive Na+ channel current. In contrast, the slow inward current decayed slowly, dependent on extracellular Ca2+ (or Ba2+) concentration, and was inhibited by the Ca2+ channel blocker, nifedipine, dose dependently (10 nM-10 microM). These results suggest that the slow inward current was a Ca2+ channel current. A fast-inactivating Ca2+ channel current was not evident when Ba2+ was the charge carrier. We conclude that the major ion channels in the cell membrane of pregnant rat uterus, which generate inward currents, are TTX-sensitive fast Na+ channels and dihydropyridine-sensitive slow Ca2+ channels (L-type, high-threshold type).
Ohya
Y
Y
Department of Physiology and Biophysics, College of Medicine, University of Cincinnati, Ohio 45267-0576.
Sperelakis
N
N
D000818:Animals; D001464:Barium / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D004095:Dihydropyridines / Q000494:pharmacology; D004553:Electric Conductivity; D005071:Evoked Potentials / Q000187:drug effects; D005260:Female; D008564:Membrane Potentials / Q000187:drug effects; D009215:Myometrium / Q000502:physiology; D011188:Potassium / Q000494:pharmacology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D051381:Rats; D012964:Sodium / Q000494:pharmacology; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D014599:Uterus / Q000502:physiology*
D015220:Calcium Channels; D004095:Dihydropyridines; D015222:Sodium Channels; D001464:Barium; D013779:Tetrodotoxin; C038806:1,4-dihydropyridine; D012964:Sodium; D011188:Potassium