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• W2111366049 abstract "Background Arachidonic acid ( AA ) and/or its enzymatic metabolites are important lipid mediators contributing to endothelium‐derived hyperpolarizing factor ( EDHF )–mediated dilation in multiple vascular beds, including human coronary arterioles ( HCA s). However, the mechanisms of action of these lipid mediators in endothelial cells ( EC s) remain incompletely defined. In this study, we investigated the role of the transient receptor potential vanilloid 4 ( TRPV 4) channel in AA ‐induced endothelial Ca 2+ response and dilation of HCA s. Methods and Results AA induced concentration‐dependent dilation in isolated HCA s. The dilation was largely abolished by the TRPV 4 antagonist RN ‐1734 and by inhibition of endothelial Ca 2+ ‐activated K + channels. In native and TRPV 4‐overexpressing human coronary artery EC s ( HCAEC s), AA increased intracellular Ca 2+ concentration ([Ca 2+ ] i ), which was mediated by TRPV 4‐dependent Ca 2+ entry. The AA ‐induced [Ca 2+ ] i increase was inhibited by cytochrome P450 ( CYP ) inhibitors. Surprisingly, the CYP metabolites of AA , epoxyeicosatrienoic acids ( EET s), were much less potent activators of TRPV 4, and CYP inhibitors did not affect EET production in HCAEC s. Apart from its effect on [Ca 2+ ] i , AA induced endothelial hyperpolarization, and this effect was required for Ca 2+ entry through TRPV 4. AA ‐induced and TRPV 4‐mediated Ca 2+ entry was also inhibited by the protein kinase A inhibitor PKI . TRPV 4 exhibited a basal level of phosphorylation, which was inhibited by PKI . Patch‐clamp studies indicated that AA activated TRPV 4 single‐channel currents in cell‐attached and inside‐out patches of HCAEC s. Conclusions AA dilates HCA s through a novel mechanism involving endothelial TRPV 4 channel‐dependent Ca 2+ entry that requires endothelial hyperpolarization, PKA ‐mediated basal phosphorylation of TRPV 4, and direct activation of TRPV 4 channels by AA ." @default.
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• W2111366049 date "2013-05-20" @default.
• W2111366049 modified "2023-10-17" @default.
• W2111366049 title "Arachidonic Acid–Induced Dilation in Human Coronary Arterioles: Convergence of Signaling Mechanisms on Endothelial TRPV4‐Mediated Ca ²⁺ Entry" @default.
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• W2111366049 doi "https://doi.org/10.1161/jaha.113.000080" @default.
• W2111366049 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3698766" @default.
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