Honoré E, Amédée T, Martin C, Dacquet C, Mironneau C, Mironneau J
Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, INSERM JF88.13, Université de Bordeaux II, France.
Pflugers Arch. 1989 Aug;414(4):477-83. doi: 10.1007/BF00585060.
Action of (+) isradipine (PN 200-110), a dihydropyridine derivative, was investigated on the Ca channel current in cultured cells obtained from the longitudinal layer of the pregnant rat myometrium (18-19 days of gestation). Under our experimental conditions, the inward current was attributed to L-type inward current since: (i) equimolar replacement of Ba for Ca induced an increase in the peak current and a decrease in inactivation rate; (ii) residual inward currents were recorded at the end of the pulse; (iii) membrane potential for mid inactivation was about -40 mV; (iv) the voltage dependencies of the peak current elicited from holding potentials of -40 mV and -80 mV were similar. The inward current could be reduced with nanomolar concentrations of (+) isradipine when cells were depolarized by pulses to positive potentials. This was characterized by a pronounced initial blockade, but by no increased in blockade when pulses were repeatedly applied at a frequency of 0.05 Hz. Using the double pulse procedure we confirmed that (+) isradipine did not bind to the open-state of the Ca channels. Voltage-dependence of (+) isradipine blockade was assessed by determining the steady-state availability of the Ca channels. From the shift of the inactivation curve in the presence of (+) isradipine we calculated a (K)I value of 130 pM. Scatchard analysis of the specific binding of (+)[3H] isradipine resulted in a linear plot, thereby indicating specific binding to a single class of sites with a dissociation constant Kd of about 100 pM.(ABSTRACT TRUNCATED AT 250 WORDS)