Vascular Smooth Muscle Adenosine Triphosphate (ATP)-Sensitive Potassium Channel and Anesthetics.
10.4097/kjae.2002.43.3.263
- Author:
Ju Tae SOHN
1
Author Information
1. Department of Anesthesiology, College of Medicine, Gyeongsang National University, Gyeongsang Institute of Health Sciences, Jinju, Korea. jtsohn@nongae.gsnu.ac.kr
- Publication Type:Review
- Keywords:
Adenosine triphosphate-sensitive potassium channel;
anesthetics;
endothelial cell;
hyperpolarization;
lemakalim
- MeSH:
Adenosine Triphosphate*;
Adenosine*;
Anesthetics*;
Anesthetics, Intravenous;
Anoxia;
Blood Vessels;
Calcium;
Calcium Channels;
Cardiovascular Diseases;
Coronary Vessels;
Cromakalim;
Endothelial Cells;
Enflurane;
Epoprostenol;
Halothane;
Humans;
Hypertension;
Hypotension;
Ischemia;
Isoflurane;
KATP Channels;
Membranes;
Muscle, Smooth, Vascular*;
Nitric Oxide;
Perfusion;
Potassium Channels*;
Potassium*;
Pulmonary Circulation;
Relaxation;
Signal Transduction;
Vascular Diseases;
Vasodilation
- From:Korean Journal of Anesthesiology
2002;43(3):263-273
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Adenosine triphosphate-sensitive potassium channel (KATP channel) closed by intracellular adenosine triphosphate (ATP) appears widely distributed in the vascular system. Activation of vascular smooth muscle KATP channel with hyperpolarizing agents such as lemakalim results in membrane hyperpolarization, a consequent reduction in calcium influx through voltage-dependent calcium channel, and leads to vessel relaxation. In contrast to KATP channel activation in vascular smooth muscle cell, KATP channel-induced hyperpolarization of endothelial cells results in an increase in calcium influx, which could stimulate the production of nitric oxide and prostacyclin from the endothelial cell. KATP channels response to change in the cellular metabolic status like ischemia and hypoxia, and are the target of a variety of synthetic and endogenous vasoactive substance. KATP channel openers are used as therapeutic agent for cardiovascular disease. Endogenous KATP channel-induced vasodilation is functionally important because it has been shown to modulate the pulmonary vasoconstrictor response to hypoxia and systemic hypotension in the pulmonary circulation, enhance tissue perfusion in response to hypoxia and severe hypotension in the systemic circulation. In virtro, halothane and intravenous anesthetics attenuated KATP channel agonist, lemaklim-induced vasodilation. The coronary vasodilation by volatile anesthetics such as isoflurane, enflurane and halothane was associated with activation of KATP channel in coronary artery. Further investigation is required to determine signal transduction pathway in detail stimulated by KATP channel agonist in human blood vessel and effect of anesthetics on the KATP channel-induced signal transduction, and role of KATP channel of pathophysiology of vascular disease such as hypertension, angina.
