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Title: Ca(2+) dependent but PKC independent signalling mediates UTP induced contraction of rat mesenteric arteries
Authors: Panhwar, Fouzia
Rainbow, Richard D.
Jackson, Robert
Davies, Noel Wyn
First Published: 10-Oct-2015
Publisher: Japanese Society of Smooth Muscle Research
Citation: Journal of Smooth Muscle Research, 2015, 51 (0), pp. 58-69
Abstract: Uridine triphosphate (UTP) can be released from damaged cells to cause vasoconstriction. Although UTP is known to act through P2Y receptors and PLC activation in vascular smooth muscle, the role of PKC in generating the response is somewhat unclear. Here we have used Tat-linked membrane permeable peptide inhibitors of PKC to assess the general role of PKC and also of specific isoforms of PKC in the UTP induced contraction of rat mesenteric artery. We examined the effect of PKC inhibition on UTP induced contraction, increased cytoplasmic Ca(2+) and reduction of K(+) currents and found that PKC inhibition caused a relatively small attenuation of contraction but had little effect on changes in cytoplasmic Ca(2+). UTP attenuation of both voltage-gated (Kv) and ATP-dependent (KATP) K(+) currents was abolished when intracellular Ca(2+) was decreased from 100 to 20 nM. PKC inhibition reduced slightly the ability of UTP to attenuate Kv currents but had no effect on KATP current inhibition. In conclusion, both UTP induced contraction of mesenteric artery and the inhibition of Kv and KATP currents of mesenteric artery smooth muscle cells by UTP are relatively independent of PKC activation; furthermore, the inhibition of both Kv and KATP currents requires intracellular Ca(2+).
DOI Link: 10.1540/jsmr.51.58
eISSN: 1884-8796
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2015. The Japan Society of Smooth Muscle Research. The publisher has the copyright of the articles published in the Journal. All articles are distributed under the terms of CC BY-NC-ND ( defined by the Creative Commons Attribution License, which is allowing others to download the material, modify it slightly and share it (either whole or parts of it) with others without any permission as long as they credit the original source and indicate if changes were made, but they can't use the material commercially.
Appears in Collections:Published Articles, Dept. of Cardiovascular Sciences

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