Referenced in: none

Automatically associated channels: TRP , TRPA , TRPA1 , TRPV , TRPV3 , TRPV4

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

Authors: Timothy V Murphy, Arjna Kanagarajah, Sianne Toemoe, Paul P Bertrand, T Hilton Grayson, Fiona C Britton, Leo Leader, Sevvandi Senadheera, Shaun L Sandow

Journal, date & volume: Vascul. Pharmacol., 2016 Apr 9 , ,

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/27073026

Abstract
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.