Abstract
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.
