IONIC CURRENTS AND INHIBITORY EFFECTS OF GLIBENCLAMIDE IN SEMINAL-VESICLE SMOOTH-MUSCLE CELLS

1 Whole-cell voltage-clamp recordings were made from smooth muscle cel ls isolated from guinea-pig seminal vesicle. 2 When the recording pipe tte solution contained 130 mM KCl and a low concentration of EGTA (0.2 mM), a dominant outward current was elicited by depolarization to pos itive of -30 mV from a holding potential of -50 mV. The current was no n-inactivating, stimulated by intracellular Ca2+ and blocked by bath-a pplied 1 mM tetraethylammonium but not 1 mM 3,4 diaminopyridine. 3 If 10 mM EGTA was added to the KCl pipette solution and the holding poten tial was -50 mV, or more negative, the major current elicited by depol arization to positive of -30 mV was an A-type K+-current. This current inactivated rapidly (within 100 ms) and was blocked by bath-applied 1 mM 3,4-diaminopyridine but not 10 mM tetraethylammonium. 4 An inward voltage-gated Ca channel current was observed on depolarization to pos itive of -30 mV with 1.5 mM Ca2+ or 10 mM Ba2+ in the bath solution an d when Cs+ replaced K+ in the pipette. The Ba2+-current was shown to b e abolished by bath-applied 100 mu M Cd2+ and inhibited by 90% by 1 mu M nifedipine, and thus appeared to be carried by L-type Ca channels. 5 High concentrations of glibenclamide (10-500 mu M) inhibited A-type K+-current, Ba2+-current and contraction of the whole tissue induced b y noradrenaline or electrical field stimulation. 6 From these data we suggest that seminal vesicle smooth muscle cells express Ca2+-dependen t K channels, A-type K channels and L-type Ca channels which are inhib ited by tetraethylammonium, 3,4-diaminopyridine and nifedipine, respec tively. In addition, an unexpected relaxant effect of high concentrati ons of glibenclamide may be explained by inhibition of the Ca channels .