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Influence of chronic hypoxia on the contributions of non‐inactivating and delayed rectifier K currents to the resting potential and tone of rat pulmonary artery smooth muscle
Author(s) -
Osipenko O. N.,
Alexander D.,
MacLean M. R.,
Gurney A. M.
Publication year - 1998
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0702006
Subject(s) - hypoxia (environmental) , cardiology , pulmonary artery , medicine , muscle tone , resting potential , potassium channel , electrophysiology , anatomy , chemistry , endocrinology , physical medicine and rehabilitation , oxygen , organic chemistry
Exposing rats to chronic hypoxia increased the 4‐aminopyridine (4‐AP) sensitivity of pulmonary arteries. 1 m m 4‐AP caused smooth muscle cell depolarization and contraction in arteries from hypoxic rats, but had little effect in age‐matched controls. Chronic hypoxia downregulated delayed rectifier K + current ( I K(V) ), which was nearly 50% blocked by 1 m m 4‐AP, and non‐inactivating K + current ( I K(N) ), which was little affected by 1 m m 4‐AP. The results suggest that I K(N) determines resting potential in control rats and that its downregulation following hypoxia leads to depolarization, which activates I K(V) and increases its contribution to resting potential. The hypoxia‐induced increase in 4‐AP sensitivity thus reflects a switch in the major K + current determining resting potential, from I K(N) to I K(V) . This has important implications for the actions and specificity of pulmonary vasodilator drugs. British Journal of Pharmacology (1998) 124 , 1335–1337; doi: 10.1038/sj.bjp.0702006