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Contractile and electrophysiological properties of pulmonary artery smooth muscle are not altered in TASK‐1 knockout mice
Author(s) -
Manoury Boris,
Lamalle Caroline,
Oliveira Roberta,
Reid Joy,
Gurney Alison M.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.206748
Subject(s) - nifedipine , electrical impedance myography , tetraethylammonium , isometric exercise , medicine , chemistry , membrane potential , patch clamp , channel blocker , electrophysiology , endocrinology , pulmonary artery , biophysics , anatomy , cardiology , biology , vasodilation , potassium , organic chemistry , calcium
Non technical summary Contraction of the muscle in the walls of blood vessels is controlled by the movement of ions into or out of the muscle cells, through proteins called ion channels. By allowing potassium (K + ) to leave the cell, K + ‐selective ion channels keep arteries dilated. In the pulmonary artery, which carries blood to the lung for gas exchange, a type of K + channel called TASK‐1 is thought to play an important role in this regulation, but we observed that the pulmonary arteries from mice that lack the TASK‐1 protein do not display any altered properties compared to wild‐type (normal) mice. We found, however, that the pattern of K + flux in muscle cells from mouse pulmonary artery is different from that of other species, including human. Our results question the use of mouse as a model for human pulmonary artery.