z-logo
Premium
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.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here