Genetic Ablation of Ca V 3.2 Channels Enhances the Arterial Myogenic Response by Modulating the RyR-BK Ca Axis
Author(s) -
Osama F. Harraz,
Suzanne E. Brett,
Anil Zechariah,
Monica Romero,
José L. Puglisi,
Sean M. Wilson,
Donald G. Welsh
Publication year - 2015
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.115.305736
Subject(s) - electrical impedance myography , mesenteric arteries , ryanodine receptor , myogenic contraction , vasoconstriction , vascular smooth muscle , constriction , medicine , vasodilation , myocyte , chemistry , anatomy , cardiology , artery , receptor , smooth muscle
In resistance arteries, there is an emerging view that smooth muscle CaV3.2 channels restrain arterial constriction through a feedback response involving the large-conductance Ca(2+)-activated K(+) channel (BKCa). Here, we used wild-type and CaV3.2 knockout (CaV3.2(-/-)) mice to definitively test whether CaV3.2 moderates myogenic tone in mesenteric arteries via the CaV3.2-ryanodine receptor-BKCa axis and whether this regulatory mechanism influences blood pressure regulation.
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