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K2P‐like current in freshly dissociated mouse thoracic aorta: the impact on thoracic aorta diameter
Author(s) -
Bychkov Rostislav,
Hayoz Sandébastien,
Soliman Youssef,
Cubano Luis,
Maldonado Hector
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.985.2
Subject(s) - glibenclamide , tetraethylammonium , vasodilation , apamin , chemistry , purinergic receptor , biophysics , potassium channel , membrane potential , medicine , p2y receptor , endocochlear potential , thoracic aorta , patch clamp , aorta , endocrinology , receptor , biochemistry , potassium , guinea pig , biology , organic chemistry , diabetes mellitus
Background It was suggested that K + channels family identified as "two‐pore potassium channels (K2P)" function as leak K + efflux that regulates membrane potential complementary to Ca 2+ , ATP and voltage dependent K + channels. Does opening of K2P channels dilate vascular beds, or do they tune membrane potential only? Methods and results Patch‐clamp technique was used to record an ATP‐γs elicited delayed K + ‐current in freshly dissociated myocytes. This current was not inhibited by a "cocktail" of K + channels blockers (TEA, 4AP, charibdotoxin, apamin, glibenclamide). Tested purinergic agonists (ATP, UTP) – except for ADP ‐ activated delayed K + ‐current indicating that at least P2Y11 receptor stimulates delayed K + ‐current. 12,13‐didecanoate also stimulated this current. ATPγs‐elicited K + ‐current amplitude decreased in staurosporine and G6850 pretreated cells. Acid pH (7 and 6) inhibited when basic pH (8) stimulated amplitude of ATPγs‐elicited K + ‐current. ATP‐γs produced a vasodilation in endothelium‐denuded thoracic aorta rings contracted by the K + ‐channels blockers and pre‐treated by carbenoxolone. Vasodilation was inhibited by acid pH (6). Conclusions Our results demonstrate that ATP‐γs dilates pre‐stretched thoracic aorta rings via stimulation of pH sensitive K + ‐current through P2Y receptors. Taken together our data provide new cellular mechanism of vasoregulation via K2P‐like channels.