Document Detail

Simultaneous inhibition of TXA(2) and PGI(2) synthesis increases NO release in mesenteric resistance arteries from cirrhotic rats.
MedLine Citation:
PMID:  20459396     Owner:  NLM     Status:  MEDLINE    
Our present study examines, in mesenteric resistance arteries, possible vasodilation alterations, and the role of NO and COX (cyclo-oxygenase) derivatives, in cirrhosis. The vasodilator response to acetylcholine was analysed in segments from control and cirrhotic rats. The effects of the non-specific COX inhibitor indomethacin, the specific COX-1 inhibitor SC-560 and the specific COX-2 inhibitor NS-398 were analysed in segments from both groups of rats. NO release was measured, and eNOS [endothelial NOS (NO synthase)], phospho-eNOS, iNOS (inducible NOS), COX-1 and COX-2 protein expression was also analysed. The effects of the TP receptor [TXA2 (thromboxane A(2)) receptor] antagonist SQ 29548, the TXA(2) synthesis inhibitor furegrelate, the PGI(2) (prostaglandin I(2)) synthesis inhibitor TCP (tranylcypromine) or TCP+furegrelate were only determined in segments from cirrhotic rats. The vasodilator response to acetylcholine was higher in segments from cirrhotic rats. Indomethacin, SC-560 and NS-398 did not modify the vasodilator response in control rats; however, indomethacin, NS-398 and TCP+furegrelate increased, whereas SC-560 did not modify and SQ 29548, furegrelate or TCP decreased, the vasodilator response to acetylcholine in cirrhotic rats. NO release was higher in cirrhotic rats. Furegrelate decreased, whereas TCP+furegrelate increased, the NO release in segments from cirrhotic rats. eNOS and COX-1 protein expression was not modified, whereas phosho-eNOS, iNOS and COX-2 protein expression was higher in cirrhotic rats. Therefore the increase in iNOS expression and eNOS activity may mediate increases in endothelial NO release. The COX-2 derivatives TXA(2) and PGI(2) may act simultaneously, producing a compensatory effect that reduces NO release and may limit the hyperdynamic circulation.
Fabiano E Xavier; Javier Blanco-Rivero; Esther Sastre; Lina Badimón; Gloria Balfagón
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-25
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  119     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-06-25     Completed Date:  2010-09-16     Revised Date:  2010-09-23    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  283-92     Citation Subset:  IM    
Departamento de Fisiologia e Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Pernambuco, Recife 50670-420, Brazil.
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MeSH Terms
Blood Pressure / physiology
Body Weight / physiology
C-Reactive Protein / metabolism
Lipid Metabolism / physiology
Liver / pathology
Liver Cirrhosis, Experimental / metabolism*,  physiopathology
Mesenteric Arteries / metabolism*
Nitric Oxide / metabolism*
Organ Size / physiology
Prostaglandins / metabolism
Prostaglandins A / biosynthesis,  physiology*
Rats, Sprague-Dawley
Spleen / pathology
Superoxides / metabolism
Thromboxane A2 / biosynthesis,  physiology*
Vasodilation / physiology
Reg. No./Substance:
0/Prostaglandins; 0/Prostaglandins A; 10102-43-9/Nitric Oxide; 11062-77-4/Superoxides; 13345-50-1/prostaglandin A2; 57576-52-0/Thromboxane A2; 9007-41-4/C-Reactive Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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