Hypoxic Pulmonary Vasoconstriction and Change in Outward K Current in Pulmonary Arterial Smooth Muscle Cell of the Rabbit.
- Author:
Dae Kyu SONG
1
;
Myoung Kyu PARK
Author Information
1. Department of Physiology, Keimyung University School of Medi-cine, Taegu.
- Publication Type:Original Article
- Keywords:
Hypoxic pulmonary vasoconstriction;
Outward K current;
Redox;
Pulmonary artery smooth muscle
- MeSH:
Ammonium Compounds;
Anoxia;
Arteries;
Calcium;
Dithiothreitol;
Ion Channels;
Kinetics;
Membrane Potentials;
Membranes;
Muscle, Smooth*;
Myocytes, Smooth Muscle*;
Oxidation-Reduction;
Patch-Clamp Techniques;
Pulmonary Artery;
Vasoconstriction*;
Vasodilation
- From:Korean Journal of Aerospace and Environmental Medicine
1999;9(2):171-175
- CountryRepublic of Korea
- Language:Korean
-
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.
