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Light–dependent effects of zinc protoporphyrin IX on endothelium–dependent relaxation resistant to NoM–nitro–L–arginine

ZYGMUNT, P. M. LU orcid ; HÖGESTÄTT, E. D. LU and GRUNDEMAR, L. LU (1994) In Acta Physiologica Scandinavica 152(2). p.137-143
Abstract

Acetylcholine (ACh) induces an Nω–nitro–L–arginine (L–NOARG)–resistant relaxation and hyperpolarization in the rat isolated hepatic artery. The possibility that carbon monoxide (CO) produced by haem oxygenase (HO) is an endogenous mediator of this response was investigated. Exogenously applied CO evoked a concentration–dependent relaxation, and the CO ‘scavenger’ oxyhaemoglobin (10μM) reduced the maximum ACh–induced relaxation by 25%. The HO inhibitor zinc protoporphyrin IX (ZnPP, 10 μM virtually abolished the ACh–induced relaxation in experiments carried out under ordinary light conditions. However, ZnPP did not affect the ACh–induced relaxation under dark conditions, even after exposure of ZnPP to intense light before the... (More)

Acetylcholine (ACh) induces an Nω–nitro–L–arginine (L–NOARG)–resistant relaxation and hyperpolarization in the rat isolated hepatic artery. The possibility that carbon monoxide (CO) produced by haem oxygenase (HO) is an endogenous mediator of this response was investigated. Exogenously applied CO evoked a concentration–dependent relaxation, and the CO ‘scavenger’ oxyhaemoglobin (10μM) reduced the maximum ACh–induced relaxation by 25%. The HO inhibitor zinc protoporphyrin IX (ZnPP, 10 μM virtually abolished the ACh–induced relaxation in experiments carried out under ordinary light conditions. However, ZnPP did not affect the ACh–induced relaxation under dark conditions, even after exposure of ZnPP to intense light before the preincubation period. Biliverdin (0.1 mM), a feedback inhibitor of HO, was also inactive under dark conditions, and the HO substrate haematin (0.1 mM) did not facilitate the ACh–induced relaxation. The relaxation induced by the nitric oxide (NO) donor 3–morpholino–sydnonimin was not affected by ZnPP in the presence of light. However, ZnPP inhibited the relaxation evoked by the potassium channel opener levcromakalim and the tonic component of the contractile response to 60 mM potassium, indicating that ZnPP has effects distinct from HO inhibition in the presence of light. ZnPP should therefore be protected from light when used to inhibit HO–mediated CO formation. The results do not suggest that CO generated by HO mediates the endothelium–dependent, L–NOARG–resistant relaxation induced by ACh in the rat hepatic artery.

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author
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organization
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type
Contribution to journal
publication status
published
subject
keywords
blood vessels, carbon monoxide, endothelium, haem oxygenases, metalloporphyrins, nitric oxide, relaxation, zinc protoporphyrin
in
Acta Physiologica Scandinavica
volume
152
issue
2
pages
7 pages
publisher
Wiley-Blackwell
external identifiers
  • scopus:0028072553
  • pmid:7839858
ISSN
0001-6772
DOI
10.1111/j.1748-1716.1994.tb09793.x
language
English
LU publication?
yes
id
1bdd59cb-d6ae-48a8-a85f-1aa4848a4852
date added to LUP
2019-05-31 21:41:47
date last changed
2024-01-01 09:00:32
@article{1bdd59cb-d6ae-48a8-a85f-1aa4848a4852,
  abstract     = {{<p>Acetylcholine (ACh) induces an Nω–nitro–L–arginine (L–NOARG)–resistant relaxation and hyperpolarization in the rat isolated hepatic artery. The possibility that carbon monoxide (CO) produced by haem oxygenase (HO) is an endogenous mediator of this response was investigated. Exogenously applied CO evoked a concentration–dependent relaxation, and the CO ‘scavenger’ oxyhaemoglobin (10μM) reduced the maximum ACh–induced relaxation by 25%. The HO inhibitor zinc protoporphyrin IX (ZnPP, 10 μM virtually abolished the ACh–induced relaxation in experiments carried out under ordinary light conditions. However, ZnPP did not affect the ACh–induced relaxation under dark conditions, even after exposure of ZnPP to intense light before the preincubation period. Biliverdin (0.1 mM), a feedback inhibitor of HO, was also inactive under dark conditions, and the HO substrate haematin (0.1 mM) did not facilitate the ACh–induced relaxation. The relaxation induced by the nitric oxide (NO) donor 3–morpholino–sydnonimin was not affected by ZnPP in the presence of light. However, ZnPP inhibited the relaxation evoked by the potassium channel opener levcromakalim and the tonic component of the contractile response to 60 mM potassium, indicating that ZnPP has effects distinct from HO inhibition in the presence of light. ZnPP should therefore be protected from light when used to inhibit HO–mediated CO formation. The results do not suggest that CO generated by HO mediates the endothelium–dependent, L–NOARG–resistant relaxation induced by ACh in the rat hepatic artery.</p>}},
  author       = {{ZYGMUNT, P. M. and HÖGESTÄTT, E. D. and GRUNDEMAR, L.}},
  issn         = {{0001-6772}},
  keywords     = {{blood vessels; carbon monoxide; endothelium; haem oxygenases; metalloporphyrins; nitric oxide; relaxation; zinc protoporphyrin}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{2}},
  pages        = {{137--143}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Acta Physiologica Scandinavica}},
  title        = {{Light–dependent effects of zinc protoporphyrin IX on endothelium–dependent relaxation resistant to NoM–nitro–L–arginine}},
  url          = {{http://dx.doi.org/10.1111/j.1748-1716.1994.tb09793.x}},
  doi          = {{10.1111/j.1748-1716.1994.tb09793.x}},
  volume       = {{152}},
  year         = {{1994}},
}