Interaction of nitric oxide with calcium in the mesenteric bed of bile duct‐ligated rats

We have analysed the interaction of NO with calcium in order to study the molecular mechanisms responsible for the vascular hyporesponse of liver cirrhosis. The experiments have been performed in the isolated and perfused mesenteric arterial bed of rats with bile duct ligation (BDL) and their contro...

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Bibliographic Details
Published in:British journal of pharmacology 2002-01, Vol.135 (2), p.489-495
Main Authors: Nadal, F Javier A, Atucha, Noemí M, Iyu, David, García‐Estañ, Joaquín
Format: Article
Language:English
Subjects:
Animals
bile duct ligation
Bile Ducts - drug effects
Bile Ducts - metabolism
Biological and medical sciences
calcium
Calcium - metabolism
Calcium Chloride - pharmacology
Calcium Signaling - drug effects
Calcium Signaling - physiology
Dose-Response Relationship, Drug
Gastroenterology. Liver. Pancreas. Abdomen
Ligation
liver cirrhosis
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
Mesenteric Arteries - drug effects
Mesenteric Arteries - metabolism
methoxamine
Methoxamine - pharmacology
Nitric oxide
Nitric Oxide - metabolism
Other diseases. Semiology
Perfusion
potassium chloride
Rats
Rats, Sprague-Dawley
vascular reactivity
Vasoconstrictor Agents - pharmacology
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Summary:We have analysed the interaction of NO with calcium in order to study the molecular mechanisms responsible for the vascular hyporesponse of liver cirrhosis. The experiments have been performed in the isolated and perfused mesenteric arterial bed of rats with bile duct ligation (BDL) and their controls. While perfusing the vessels with normal Krebs, methoxamine (MTX) or KCl produced a lower pressor response in the BDL mesenteries. The NO synthesis inhibitor Nw‐nitro‐L‐arginine (NNA) potentiated those responses and abolished the differences between groups. The administration of MTX under perfusion with zero calcium‐Krebs, to analyse the intracellular release of calcium, also induced a lower response in the BDL mesenteries and NNA potentiated and normalized the response. To investigate calcium entry, the vessels were perfused with zero‐calcium Krebs containing high potassium to open voltage‐dependent calcium channels. Then, the addition of calcium (10−1–3×10−3 M) produced a lower pressor response in the BDL vessels, that was corrected by NNA. To study calcium entry through receptor‐operated channels, the vessels were perfused with zero‐calcium Krebs containing MTX. The addition of calcium elevated the perfusion pressure less in the BDL mesenteries than in the control and NNA potentiated the responses and eliminated the between groups differences. When calcium entry through both voltage‐ and receptor‐operated channels was simultaneously analysed, similar results were obtained. In the mesenteric bed of bile duct ligated rats, an excess of nitric oxide affects vascular calcium regulation through an interaction with both calcium entry and intracellular calcium release. British Journal of Pharmacology (2002) 135, 489–495; doi:10.1038/sj.bjp.0704504
ISSN:0007-1188
1476-5381
DOI:10.1038/sj.bjp.0704504