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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Abstract
Half decay time of the K-induced contracture of rabbit main pulmonary artery following pretreatment with Ca-free EGTA [ethylene glycol bis (.beta.-aminoethyl ether) N,N,N,N''-tetraacetic acid] containing solution was 110 s. A Ca-free K-solution did not generate contraction, while noradrenaline [norepinephrine], acetylcholine and prostaglandin F2.alpha.-containing solution did evoke contracture. Decays of the chemically induced mechanical response in Ca-free solution against the exposure times was classified into 3 components (2 min, 28 min and over 100 min, respectively). When 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 118 mM K+. When the membrane potential was clamped at the resting level before, during and after application of the excess K+, the excess K+ still evoked contracture. Amplitudes of contracture depended on extracellular K concentration [K]o. The effects of various [K]o on the length constant of the tissue were also observed in relation to the clamping condition. The mechanical response of the pulmonary artery induced by excess K was mainly due to influx of Ca2+, and depolarization played only a minor role. Release of stored Ca by depolarization was not an essential factor in generation of K-induced contracture in this tissue.