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36 YOHIMBINE EFFECTS ON MYOCARDIAL VOLTAGE-DEPENDENT CATION CHANNELS. J. Azuma* and N. Sperelakis. Department of Phy- siology, University of Virginia, Charlottesville, Va. U.S.A. *Third Department of Internal Medicine, Osaka University Medical School, Osaka, Japan. Yohimbine, a vasodilator, was tested for its effects on the fast Na + and slow Ca2+-Na + channels in perfused chick hearts (ventricular cells). Both fast and slow channels were blocked by yohimbine. The action potential rate of rise was depressed and reduced in amplitude, and the dura- tion was prolonged. The fast Na + channels were more sensi- tive to blockade by yohimbine (10-4 M) than the slow chan- nels (>10 -3 M) induced by isoproterenol in tetrodotoxin or high K +- blocked hearts. The contractions were blocked simultaneously with the slow channels. Low concentrations of yohimbine (10 -5 M) sometimes showed a small positive ino- tropic effect concomitant with induction of slow Ca2+ -Na + channels. This action was not prevented by propranolol, but was depressed by Mn 2+ or verapamil. These results sug- gest that yohimbine has a dual action on the myocardium: low concentrations induce slow channels, whereas high con- centrations block them. THE MECHANISM OF OVERDRIVE SUPPRESSION--ACTIVATION OF ELECTROGENIC SODIUM PUMP FOLLOWING OVERDRIVE. I. Kodama, Y. Hirata, S. Ando, J. Toyama, K. Yamada. Department of Respiration and Circulation, Research Institute of Envi- romental Medicine, Nagoya University, Nagoya, Japan. Effects of overdrive on maximum diastolic potential (MDP) on isolated canine Purkinje and ventricular muscle fibers were studied using microelectrode techniques. Dur- ing the overdrive stimulation MDP decreased initially but increased above control within 30 seconds. After the ces- sation of overdrive further increase in MDP was observed for about I0 seconds. This post-overdrive hyperpolariza- tion(POH) subsided gradually within 3 minutes. POH which is attributed to the activation of sodium pump, was en- hanced by increasing the rate or duration of overdrive. In the low temperature perfusate(31~ POH decreased a little in its maximum value, but it lasted longer than that in control perfusate(37~ These properties of POH were similar to those of automaticity in cardiac cells following overdrive, and may support the hypothesis that an activation of electrogenic sodium pump plays an impor- tant role in the mechanism of "overdrive suppression".

The mechanism of overdrive suppression — Activation of electrogenic sodium pump following overdrive

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YOHIMBINE EFFECTS ON MYOCARDIAL VOLTAGE-DEPENDENT CATION CHANNELS. J. Azuma* and N. Sperelakis. Department of Phy- siology, University of Virginia, Charlottesville, Va. U.S.A. *Third Department of Internal Medicine, Osaka University Medical School, Osaka, Japan.

Yohimbine, a vasodilator, was tested for its effects on the fast Na + and slow Ca2+-Na + channels in perfused chick hearts (ventricular cells). Both fast and slow channels were blocked by yohimbine. The action potential rate of rise was depressed and reduced in amplitude, and the dura- tion was prolonged. The fast Na + channels were more sensi- tive to blockade by yohimbine (10 -4 M) than the slow chan- nels (>10 -3 M) induced by isoproterenol in tetrodotoxin or high K +- blocked hearts. The contractions were blocked simultaneously with the slow channels. Low concentrations of yohimbine (10 -5 M) sometimes showed a small positive ino- tropic effect concomitant with induction of slow Ca2+ -Na + channels. This action was not prevented by propranolol, but was depressed by Mn 2+ or verapamil. These results sug- gest that yohimbine has a dual action on the myocardium: low concentrations induce slow channels, whereas high con- centrations block them.

THE MECHANISM OF OVERDRIVE SUPPRESSION--ACTIVATION OF ELECTROGENIC SODIUM PUMP FOLLOWING OVERDRIVE. I. Kodama, Y. Hirata, S. Ando, J. Toyama, K. Yamada. Department of Respiration and Circulation, Research Institute of Envi- romental Medicine, Nagoya University, Nagoya, Japan.

Effects of overdrive on maximum diastolic potential (MDP) on isolated canine Purkinje and ventricular muscle fibers were studied using microelectrode techniques. Dur- ing the overdrive stimulation MDP decreased initially but increased above control within 30 seconds. After the ces- sation of overdrive further increase in MDP was observed for about I0 seconds. This post-overdrive hyperpolariza- tion(POH) subsided gradually within 3 minutes. POH which is attributed to the activation of sodium pump, was en- hanced by increasing the rate or duration of overdrive. In the low temperature perfusate(31~ POH decreased a little in its maximum value, but it lasted longer than that in control perfusate(37~ These properties of POH were similar to those of automaticity in cardiac cells following overdrive, and may support the hypothesis that an activation of electrogenic sodium pump plays an impor- tant role in the mechanism of "overdrive suppression".