Effects of Inducible Nitric Oxide Synthase Inhibition on the Rat Tail Vascular Bed Reactivity Three Days After Myocardium Infarction

The acute phase of myocardial infarction promotes an inflammatory response that stimulates inducible nitric oxide synthase (iNOS). We investigated the iNOS role on the rat tail vascular bed reactivity 3 days after myocardial infarction. Vasodilator and vasoconstrictor responses were determined in is...

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Bibliographic Details
Published in:	Journal of cardiovascular pharmacology Vol. 45; no. 4; pp. 321 - 326
Main Authors:	Sartório, Carmem Luíza, Pinto, Valber Dias, Cutini, Gustavo Julio de Salles, Vassallo, Dalton Valentim, Stefanon, Ivanita
Format:	Journal Article
Language:	English
Published:	United States Lippincott Williams & Wilkins, Inc 01-04-2005
Subjects:	Animals Dose-Response Relationship, Drug Enzyme Inhibitors - pharmacology In Vitro Techniques Male Myocardial Infarction - enzymology Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - biosynthesis Nitric Oxide Synthase Type II Rats Rats, Wistar Tail - blood supply Tail - drug effects Tail - enzymology Vasodilation - drug effects Vasodilation - physiology
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Summary:	The acute phase of myocardial infarction promotes an inflammatory response that stimulates inducible nitric oxide synthase (iNOS). We investigated the iNOS role on the rat tail vascular bed reactivity 3 days after myocardial infarction. Vasodilator and vasoconstrictor responses were determined in isolated caudal vascular beds from Wistar rats 3 days after coronary artery ligation (CAL) and sham-operated animals (SHAM). Rats were treated with the iNOS inhibitor S-methylisothiourea sulfate (SMT), 5 mg Kg day, i.p. or placebo. Concentration of plasma nitrite/nitrate (NOx) and the expression of iNOS mRNA in tail arteries were evaluated. The CAL group showed increased maximal vasoconstrictor response to phenylephrine (SHAM= 241 ± 8; CAL= 288 ± 13 mm Hg, P < 0.05) and SMT treatment normalized this effect (CAL-SMT = 253 ± 7 mm Hg, P < 0.05). The sensitivity to acetylcholine was reduced in the CAL group, but SMT treatment did not alter this response. The plasma NOx and iNOS mRNA expression in tail arteries were increased in CAL rats. SMT treatment reduced the plasma NOx in the CAL group and the arterial expression of iNOS mRNA in SHAM and CAL group. In conclusion, iNOS inhibition prevented the increased phenylephrine reactivity in rat caudal vascular beds 3 days after myocardial infarction.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0160-2446 1533-4023
DOI:	10.1097/01.fjc.0000156822.58081.be