저산소성 폐혈관 수축과 토끼 폐동맥 평활근 세포의 외향성 칼륨 전류의 변화

Abstract

Hypoxic pulmonary vasoconstriction (HPV) is well-known characteristic of pulmonary artery during the exposure of low O2 conditions. It has been demonstrated that hypoxia inhibits an outward K current, thus causing membrane depolarization and calcium influx through the voltage-dependent Ca channels in pulmonary artery smooth muscle cells. Hypoxia induces a reducing condition within the cell. The change of the redox (reduction and oxidation) state in the cells can also modulate the kinetics of ion channels which is influential to membrane potential. Under the assumption that the reducing milieu during hypoxia inhibits the outward K current and vasodilation, we have studied the effects of redox state on the K currents in the pulmonary artery smooth muscle cells of the rabbit using patch-clamp technique. The outward K current was induced by depolarization from holding potential -80 mV. A reducing agent dithiothreitol inhibited the outward K current, whereas an oxidizing agent dithio-bis (5-nitropyridine) potentiated it. The tetraethyl ammonium, a K channel blocker, mainly suppressed the inactivating component of the K current. Another blocker of voltage dependent K channel E4031 had no effect. This results suggest that the reducing state within the cell during hypoxia modulates the outward K current, which leads vasoconstriction through depolarization and Ca influx. This may be one of mechanisms of HPV in contrast to the other arteries of the body to dilate during low O2 tension.