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TRPV3 expression and vasodilator function in isolated uterine radial arteries from non-pregnant and pregnant rats
Journal article   Peer reviewed

TRPV3 expression and vasodilator function in isolated uterine radial arteries from non-pregnant and pregnant rats

T V Murphy, A Kanagarajah, S Toemoe, P P Bertrand, T Hilton Grayson, Fiona C Britton, Leo Leader, S Senadheera and Shaun L Sandow
Vascular Pharmacology, Vol.83, pp.66-77
2016
url
https://doi.org/10.1016/j.vph.2016.04.004View
Published Version

Abstract

TRPV3 carvacrol uterus radial artery pregnancy
This study investigated the expression and function of transient receptor potential vanilloid type-3 ion channels (TRPV3) in uterine radial arteries isolated from non-pregnant and twenty-day pregnant rats. Immunohistochemistry (IHC) suggested TRPV3 is primarily localized to the smooth muscle in arteries from both non-pregnant and pregnant rats. IHC using C′ targeted antibody, and qPCR of TRPV3 mRNA, suggested pregnancy increased arterial TRPV3 expression. The TRPV3 activator carvacrol caused endothelium-independent dilation of phenylephrine-constricted radial arteries, with no difference between vessels from non-pregnant and pregnant animals. Carvacrol-induced dilation was reduced by the TRPV3-blockers isopentenyl pyrophosphate and ruthenium red, but not by the TRPA1 or TRPV4 inhibitors HC-030031 or HC-067047, respectively. In radial arteries from non-pregnant rats only, inhibition of NOS and sGC, or PKG, enhanced carvacrol-mediated vasodilation. Carvacrol-induced dilation of arteries from both non-pregnant and pregnant rats was prevented by the IKCa blocker TRAM-34. TRPV3 caused an endothelium-independent, IKCa-mediated dilation of the uterine radial artery. NO-PKG-mediated modulation of TRPV3 activity is lost in pregnancy, but this did not alter the response to carvacrol.

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