caa a22 4500 469079207 CHVBK 20180323132944.0 cr unu---uuuuu 170328e19920301xx s 000 0 eng 10.1007/BF00168696 doi (NATIONALLICENCE)springer-10.1007/BF00168696 Sänchez-Chapula Jose Centro de Investigaciones Biomédicas de la Universidad de Colima, Apartado Postal 199, MEX-28010, Colima, Col. México aut Effects of metoprolol on action potential and membrane currents in guinea-pig ventricular myocytes [Elektronische Daten] [Jose Sänchez-Chapula] Summary: The effects of the beta-adrenoceptor antagonist metoprolol on action potentials and membrane currents were studied in single guinea-pig ventricular myocytes. The experiments were carried out using the nystatin-method of whole-cell technique. This method was used in order to prevent the run-down of the calcium current. Metoprolol at concentrations of 10-100 μmol/l shortened action potential in a dose-dependent way. The drug only decreased resting membrane potential at a concentration of 100 μmol/1 in two out of five cells. Under voltage-clamp conditions, metoprolol blocked the high threshold calcium current at concentrations of 30 and 100 μmol/l to 82 ± 4% and 73 ± 5% from control, respectively. The drug decreased the inward rectifying potassium current in a concentration-dependent manner. This effect was evident for inward current at voltages negative to the apparent reversal potential and for outward current at voltages between −30 and −80 mV. This blocking effect on the inward rectifying potassium current can explain the effect on resting membrane potential. At voltages positive to −30 mV metoprolol increased a time-independent outward current. This metoprolol-enhanced outward current was blocked by barium and cesium. This result suggests that the metoprolol-enhanced current is carried by potassium. The current component enhanced by metoprolol was not sensitive to glibenclamide and tetraethylammonium applied externally, which suggests that the adenosine triphosphate-sensitive channel is not the target of metoprolol. The activation of this time-independent outward current by metoprolol and the blocking effects on the calcium current seem to explain the shortening in action potential induced by the drug. Springer-Verlag, 1992 Metoprolol nationallicence Single ventricular myocytes nationallicence Action potential nationallicence Calcium current nationallicence Potassium currents nationallicence Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 345/3(1992-03-01), 342-348 0028-1298 345:3<342 1992 345 210 https://doi.org/10.1007/BF00168696 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00168696 text/html Onlinezugriff via DOI NATIONALLICENCE 100 1- Sänchez-Chapula Jose Centro de Investigaciones Biomédicas de la Universidad de Colima, Apartado Postal 199, MEX-28010, Colima, Col. México aut NATIONALLICENCE 773 0- Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 345/3(1992-03-01), 342-348 0028-1298 345:3<342 1992 345 210 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer