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Endothelium‐dependent relaxation resistant to N/ω‐nitro‐L‐arginine in the rat hepatic artery and aorta

ZYGMUNT, P. M. LU orcid ; GRUNDEMAR, L. LU and HÖGESTÄTT, E. D. LU (1994) In Acta Physiologica Scandinavica 152(1). p.107-114
Abstract

Nitric oxide (NO)‐independent pathways contributing to acetylcholine (ACh)‐induced relaxation were examined in the rat isolated hepatic artery and aorta at low and high levels of precontraction induced by phenylephrine (PhE). In the hepatic artery, the ACh‐induced relaxation was unaffected by the NO synthase inhibitors Nw‐nitro‐L‐arginine (L‐NOARG, 0.3 mM) and Nω‐nitro‐L‐arginine methyl ester (0.1 mM) at either level of pre‐contraction. In the aorta, L‐NOARG virtually abolished the ACh‐induced relaxation at a high level, but only partially reduced the response at a low level of precontraction. Methylene blue (10 μM) and indomethacin (10 μM) did not affect the ACh‐induced relaxation in the hepatic artery. L‐NOARG completely inhibited the... (More)

Nitric oxide (NO)‐independent pathways contributing to acetylcholine (ACh)‐induced relaxation were examined in the rat isolated hepatic artery and aorta at low and high levels of precontraction induced by phenylephrine (PhE). In the hepatic artery, the ACh‐induced relaxation was unaffected by the NO synthase inhibitors Nw‐nitro‐L‐arginine (L‐NOARG, 0.3 mM) and Nω‐nitro‐L‐arginine methyl ester (0.1 mM) at either level of pre‐contraction. In the aorta, L‐NOARG virtually abolished the ACh‐induced relaxation at a high level, but only partially reduced the response at a low level of precontraction. Methylene blue (10 μM) and indomethacin (10 μM) did not affect the ACh‐induced relaxation in the hepatic artery. L‐NOARG completely inhibited the cGMP and cAMP increases induced by ACh in both types of artery. In the presence of L‐NOARG, ACh was unable to relax the hepatic artery precontracted by K+. The sensitivity to PhE was increased less by L‐NOARG (threefold) than after endothelial denudation (tenfold) in the hepatic artery, whereas no such difference was observed in the aorta. The relaxation induced by the NO donor 3‐morpholino‐sydnonimin did not differ between the arteries after endothelial denudation. These results are compatible with the existence of an endothelium‐dependent inhibitory pathway distinct from the NO and cyclooxygenase pathways. This pathway seems to contribute more to the ACh‐induced relaxation in the hepatic artery than in the aorta, whereas the opposite appears to be true for the NO pathway.

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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
acetylcholine, blood vessels, nitric oxide, vascular endothelium, vasodilation
in
Acta Physiologica Scandinavica
volume
152
issue
1
pages
8 pages
publisher
Wiley-Blackwell
external identifiers
  • pmid:7810328
  • scopus:0028101768
ISSN
0001-6772
DOI
10.1111/j.1748-1716.1994.tb09789.x
language
English
LU publication?
yes
id
37dc5466-df4f-410a-966e-fef63c027343
date added to LUP
2019-05-31 21:41:18
date last changed
2024-01-01 09:00:32
@article{37dc5466-df4f-410a-966e-fef63c027343,
  abstract     = {{<p>Nitric oxide (NO)‐independent pathways contributing to acetylcholine (ACh)‐induced relaxation were examined in the rat isolated hepatic artery and aorta at low and high levels of precontraction induced by phenylephrine (PhE). In the hepatic artery, the ACh‐induced relaxation was unaffected by the NO synthase inhibitors Nw‐nitro‐L‐arginine (L‐NOARG, 0.3 mM) and Nω‐nitro‐L‐arginine methyl ester (0.1 mM) at either level of pre‐contraction. In the aorta, L‐NOARG virtually abolished the ACh‐induced relaxation at a high level, but only partially reduced the response at a low level of precontraction. Methylene blue (10 μM) and indomethacin (10 μM) did not affect the ACh‐induced relaxation in the hepatic artery. L‐NOARG completely inhibited the cGMP and cAMP increases induced by ACh in both types of artery. In the presence of L‐NOARG, ACh was unable to relax the hepatic artery precontracted by K<sup>+</sup>. The sensitivity to PhE was increased less by L‐NOARG (threefold) than after endothelial denudation (tenfold) in the hepatic artery, whereas no such difference was observed in the aorta. The relaxation induced by the NO donor 3‐morpholino‐sydnonimin did not differ between the arteries after endothelial denudation. These results are compatible with the existence of an endothelium‐dependent inhibitory pathway distinct from the NO and cyclooxygenase pathways. This pathway seems to contribute more to the ACh‐induced relaxation in the hepatic artery than in the aorta, whereas the opposite appears to be true for the NO pathway.</p>}},
  author       = {{ZYGMUNT, P. M. and GRUNDEMAR, L. and HÖGESTÄTT, E. D.}},
  issn         = {{0001-6772}},
  keywords     = {{acetylcholine; blood vessels; nitric oxide; vascular endothelium; vasodilation}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{1}},
  pages        = {{107--114}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Acta Physiologica Scandinavica}},
  title        = {{Endothelium‐dependent relaxation resistant to N/ω‐nitro‐L‐arginine in the rat hepatic artery and aorta}},
  url          = {{http://dx.doi.org/10.1111/j.1748-1716.1994.tb09789.x}},
  doi          = {{10.1111/j.1748-1716.1994.tb09789.x}},
  volume       = {{152}},
  year         = {{1994}},
}