Arachidonic Acid–Induced Dilation in Human Coronary Arterioles: Convergence of Signaling Mechanisms on Endothelial TRPV4-Mediated Ca Entry

نویسندگان

  • Xiaodong Zheng
  • Natalya S. Zinkevich
  • Kathryn M. Gauthier
  • Yoshinori Nishijima
  • David A. Wilcox
  • David D. Gutterman
  • David X. Zhang
چکیده

TRPV4 antagonist RN-1734 and by inhibition of endothelial Ca-activated K channels. In native and TRPV4-overexpressing human coronary artery ECs (HCAECs), AA increased intracellular Ca concentration ([Ca]i), which was mediated by TRPV4-dependent Ca entry. The AA-induced [Ca]i increase was inhibited by cytochrome P450 (CYP) inhibitors. Surprisingly, the CYP metabolites of AA, epoxyeicosatrienoic acids (EETs), were much less potent activators of TRPV4, and CYP inhibitors did not affect EET

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Arachidonic Acid–Induced Dilation in Human Coronary Arterioles: Convergence of Signaling Mechanisms on Endothelial TRPV4‐Mediated Ca2+ Entry

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تاریخ انتشار 2013