創薬における薬理学の役割　抗不整脈薬の新しい展開

• 菅野 盛夫

  北海道大学医学部薬理学第二講座

書誌事項

タイトル別名

• New evolvement of antiarrhythmic drugs.
• コウ フセイミャクヤク ノ アタラシイ テンカイ
• 創薬における薬理学の役割

抄録

The Cardiac Arrhythmia Suppression Trial (CAST) casted serious doubts on the usefulness of Class I antiarrhythmic drugs, causing us to turn our attention from drugs impairing conduction of excitation in the myocardium by blocking sodium channels toward those producing increased refractoriness of myocardial cells by blocking potassium channels. This change in the direction of thinking from the “Na⁺ channel paradigm” to “K⁺ channel paradigm” resulted in the generation of newly synthetized Class III drugs that have the common electrophysiological property of suppressing outward K⁺ currents (I_K, I_K1, I_to) without affecting inward currents (I_Na, I_ca). However, their reversed use-dependence of action potential duration prolonging effect contributes to their untoward action of proarrhythmias. It is still controversial if ion channel blockers acting solely on a certain kind of ion channels are more beneficial than drugs having compound actions such as amiodarone or sotalol. Molecular biology, if combined with arrhythmology, is expected to provide new chemical and pharmacological bases for creating novel antiarrhythmic drugs.

収録刊行物

• 日本薬理学雑誌

  日本薬理学雑誌 102 (3), 215-223, 1993

  公益社団法人 日本薬理学会

キーワード

• Pharmacology

詳細情報

• CRID: 1390001204272911360
• NII論文ID: 130000760109
• NII書誌ID: AN00198335
• DOI: 10.1254/fpj.102.215
• ISSN: 13478397
• ISSN: 00155691
• NDL書誌ID: 3844436
• PubMed: 8406233
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I3844436
• Web Site: https://search.jamas.or.jp/link/ui/1994074083
• 本文言語コード: ja
• データソース種別:
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