心筋細胞の電気現象と薬物の作用

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概要

• 論文の詳細を見る

• Physiological bases of the electrical phenomena in the heart were briefly reviewed, and our studies on the developmental changes in the electrical properties of chick embryonic hearts were described. We found that, as age advances, the potassium conductance increased, resulting in the increase in the resting potential. The rising phase of the action potential of the young heart was found to be formed by the slow Na^+ channels, and that of the old heart by the fast Na^+ channels. Slow Ca^<2+> channels were found to contribute to the formation of the plateau component increasingly with age. With respect to the drug actions on the electrical properties of the cardiac muscle, the effects of antiarrhythmic agents, catecholamines and histamine were mainly described. Four proposed mechanisms of action of antiarrhythmic agents were explained from the electrophysiological basis. The actions of Class I and II agents were mainly described, which we examined most extensively. Changes in the sensitivities to catecholamines and histamine during postnatal development were examined with rats and guinea pigs, respectively. Possible correlation between the sympathetic innervation and the catecholamine sensitivity was proposed, and it was suggested that the denervation supersensitivity was possibly of the postjunctional type. Lastly, cardiac slow channel system predominantly admitting the Ca^<2+> current and its relation to the cardiac mechanical activities were reviewed briefly. Results we obtained in relation to this slow Ca^<2+> channels were described. We found the lack of parallelism between the activities of the positive inotropic agents to elicit this slow channels in the depolarized myocardium and to increase the contractile force under the normal condition where the fast Na^+ channels are functioning, and suggested that the positive inotropic effects of the drugs were not solely explained by their effects to increase the density of the slow channels.

• 公益社団法人日本薬学会の論文
• 1980-11-25

著者

• 重信 弘毅

  東京大学薬学部

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