ON THE ROLES OF CALCIUM ION DURING POTASSIUM INDUCED CONTRACTURE IN THE SMOOTH MUSCLE CELLS OF THE RABBIT MAIN PULMONARY ARTERY

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  • 伊東 祐之
    Department of Pharmacology, Faculty of Medicine, Kyushu University
  • 鈴木 光
    Department of Pharmacology, Faculty of Medicine, Kyushu University
  • 栗山 煕
    Department of Pharmacology, Faculty of Medicine, Kyushu University

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タイトル別名
  • On the Roles of Calcium Ion During Pota

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The half decay time of the K-induced contracture of rabbit main pulmonary artery following pretreatment with Ca-free EGTA containing solution was 110sec. A Ca-free K-solution did not generate contraction while noradrenaline, acetylcholine and prostaglandin F2α-containing solution did evoke contracture. The decays of the chemically induced mechanical response in Ca-free solution against the exposure times could be classified into three components (2min, 28min and over 100min, respectively).When the membrane depolarization produced by excess K+ was simulated in Krebs solution by application of current, the generated mechanical response was smaller than that produced by 118mM K+. When the membrane potential was clamped at the resting level before, during and after application of the excess K+, and excess K+ still evoked contracture. The amplitudes of contracture depended on [K]0 The effects of various [K]0 on the length constant of the tissue were also observed in relation to the clamping condition. It is postulated that the mechanical response of the pulmonary artery induced by excess K is mainly due to influx of Ca++and the depolarization plays only a minor role. This means that release of stored Ca by depolarization is not an essential factor in generation of K-induced contracture in this tissue.

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