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Induces vasodilatation of rat mesenteric artery in vitro mainly by inhibiting receptor-mediated Ca2+-influx and Ca2+-release

Cao, YX; Zheng, JP; He, JY; Li, J; Xu, Cang-Bao LU and Edvinsson, Lars LU (2005) In Archives of Pharmacal Research 28(6). p.709-715
Abstract
The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1 mu M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the alpha(1)-adrenoreceptor.... (More)
The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1 mu M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the alpha(1)-adrenoreceptor. The beta-adrenoreceptor and ATIP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and CaCl2 in Ca2+-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular Ca2+ influx through the receptor-operated calcium channels and intracellular Ca2+ release from the Ca (2+) store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular Ca2+ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated Ca2+-influx and Ca2+-release, and partly from the endothelium mediated by EDHF. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
EDHF, Ca2+, rat mesenteric artery, atropine, vasodilatation
in
Archives of Pharmacal Research
volume
28
issue
6
pages
709 - 715
publisher
Pharmaceutical Society of Korea
external identifiers
  • pmid:16042081
  • wos:000230180000012
  • scopus:24944514631
ISSN
1976-3786
language
English
LU publication?
yes
id
7b2b465d-ba1e-49ca-a4c6-362ad1e226db (old id 233982)
date added to LUP
2007-08-15 09:36:00
date last changed
2017-08-06 03:51:36
@article{7b2b465d-ba1e-49ca-a4c6-362ad1e226db,
  abstract     = {The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1 mu M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the alpha(1)-adrenoreceptor. The beta-adrenoreceptor and ATIP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and CaCl2 in Ca2+-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular Ca2+ influx through the receptor-operated calcium channels and intracellular Ca2+ release from the Ca (2+) store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular Ca2+ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated Ca2+-influx and Ca2+-release, and partly from the endothelium mediated by EDHF.},
  author       = {Cao, YX and Zheng, JP and He, JY and Li, J and Xu, Cang-Bao and Edvinsson, Lars},
  issn         = {1976-3786},
  keyword      = {EDHF,Ca2+,rat mesenteric artery,atropine,vasodilatation},
  language     = {eng},
  number       = {6},
  pages        = {709--715},
  publisher    = {Pharmaceutical Society of Korea},
  series       = {Archives of Pharmacal Research},
  title        = {Induces vasodilatation of rat mesenteric artery in vitro mainly by inhibiting receptor-mediated Ca2+-influx and Ca2+-release},
  volume       = {28},
  year         = {2005},
}