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The endothelium mediates a nitric oxide‐independent hyperpolarization and relaxation in the rat hepatic artery

ZYGMUNT, P. M. LU ; WALDECK, K. and HÖGESTÄTT, E. D. LU (1994) In Acta Physiologica Scandinavica 152(4). p.375-384
Abstract

The rat hepatic artery responds to acetylcholine (ACh) with an endothelium‐dependent relaxation, which is unaffected by nitric oxide (NO) synthase and cyclooxygenase inhibition. The purpose of this study was to investigate whether the NO‐independent relaxation is caused by hyperpolarization of the smooth muscle cells. In vessels with endothelium ACh induced a hyperpolarization in the presence of 0.3 mM Nw‐nitro‐l‐arginine (l‐NOARG) and 10μm indomethacin. The hyperpolarization, which slowly decayed after an initial maximum, generally lasted for at least 20 min. ACh in contrast to levcromakalim failed to hyperpolarize the smooth muscle cells in endothelium‐denuded vessels. In vessels contracted by phenylephrine (PhE) ACh caused a... (More)

The rat hepatic artery responds to acetylcholine (ACh) with an endothelium‐dependent relaxation, which is unaffected by nitric oxide (NO) synthase and cyclooxygenase inhibition. The purpose of this study was to investigate whether the NO‐independent relaxation is caused by hyperpolarization of the smooth muscle cells. In vessels with endothelium ACh induced a hyperpolarization in the presence of 0.3 mM Nw‐nitro‐l‐arginine (l‐NOARG) and 10μm indomethacin. The hyperpolarization, which slowly decayed after an initial maximum, generally lasted for at least 20 min. ACh in contrast to levcromakalim failed to hyperpolarize the smooth muscle cells in endothelium‐denuded vessels. In vessels contracted by phenylephrine (PhE) ACh caused a concentration‐dependent hyperpolarization and relaxation, and both events occurred over the same concentration interval. Curve fitting using the Hill equation showed a close correlation between the hyperpolarization and the relaxation. Exposure to a 30 mM K+ solution abolished the hyperpolarization and suppressed the relaxation induced by ACh. Nimodipine did not affect the ACh‐induced hyperpolarization, whereas the relaxation induced by ACh and levcromakalim, but not that evoked by the NO donor 3‐morpholino‐sydnonimin, were attenuated. Glibenclamide had no effect on the ACh‐induced hyperpolarization and relaxation, but abolished the corresponding responses to levcromakalim. The results demonstrate a NO‐independent hyperpolarization and relaxation in the rat hepatic artery. The hyperpolarization and relaxation were endothelium‐dependent, and apparently causally related to each other, since interference with the hyperpolarization or the subsequent effector pathway inhibited the relaxation.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
arteries, hyperpolarization, membrane potential, nitric oxide, relaxation, vascular endothelium
in
Acta Physiologica Scandinavica
volume
152
issue
4
pages
375 - 384
publisher
Wiley-Blackwell
external identifiers
  • scopus:0028036807
ISSN
0001-6772
DOI
10.1111/j.1748-1716.1994.tb09819.x
language
English
LU publication?
yes
id
af5c0b8e-e6d7-4c58-a1fd-3f2a9569d30b
date added to LUP
2019-05-31 21:42:06
date last changed
2019-06-18 02:19:05
@article{af5c0b8e-e6d7-4c58-a1fd-3f2a9569d30b,
  abstract     = {<p>The rat hepatic artery responds to acetylcholine (ACh) with an endothelium‐dependent relaxation, which is unaffected by nitric oxide (NO) synthase and cyclooxygenase inhibition. The purpose of this study was to investigate whether the NO‐independent relaxation is caused by hyperpolarization of the smooth muscle cells. In vessels with endothelium ACh induced a hyperpolarization in the presence of 0.3 mM Nw‐nitro‐l‐arginine (l‐NOARG) and 10μm indomethacin. The hyperpolarization, which slowly decayed after an initial maximum, generally lasted for at least 20 min. ACh in contrast to levcromakalim failed to hyperpolarize the smooth muscle cells in endothelium‐denuded vessels. In vessels contracted by phenylephrine (PhE) ACh caused a concentration‐dependent hyperpolarization and relaxation, and both events occurred over the same concentration interval. Curve fitting using the Hill equation showed a close correlation between the hyperpolarization and the relaxation. Exposure to a 30 mM K<sup>+</sup> solution abolished the hyperpolarization and suppressed the relaxation induced by ACh. Nimodipine did not affect the ACh‐induced hyperpolarization, whereas the relaxation induced by ACh and levcromakalim, but not that evoked by the NO donor 3‐morpholino‐sydnonimin, were attenuated. Glibenclamide had no effect on the ACh‐induced hyperpolarization and relaxation, but abolished the corresponding responses to levcromakalim. The results demonstrate a NO‐independent hyperpolarization and relaxation in the rat hepatic artery. The hyperpolarization and relaxation were endothelium‐dependent, and apparently causally related to each other, since interference with the hyperpolarization or the subsequent effector pathway inhibited the relaxation.</p>},
  author       = {ZYGMUNT, P. M. and WALDECK, K. and HÖGESTÄTT, E. D.},
  issn         = {0001-6772},
  keyword      = {arteries,hyperpolarization,membrane potential,nitric oxide,relaxation,vascular endothelium},
  language     = {eng},
  number       = {4},
  pages        = {375--384},
  publisher    = {Wiley-Blackwell},
  series       = {Acta Physiologica Scandinavica},
  title        = {The endothelium mediates a nitric oxide‐independent hyperpolarization and relaxation in the rat hepatic artery},
  url          = {http://dx.doi.org/10.1111/j.1748-1716.1994.tb09819.x},
  volume       = {152},
  year         = {1994},
}