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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on November 23, 2004; DOI: 10.1124/jpet.104.077701

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Received for publication September 13, 2004.
Revised November 13, 2004.
Accepted for publication November 23, 2004.

Differences in tail vascular bed reactivity in rats with and without heart failure following myocardial infarction

Raquel Binda Pereira 1*, Carmem Luiza Sartorio 1, Dalton Valentim Vassallo 1, Ivanita Stefanon 1

1 Ufes

* Address correspondence to: E-mail: raquelbinda{at}yahoo.com.br

Abstract

Myocardial infarction (MI) was induced in rats by coronary ligation to compare changes in vascular reactivity from animals that developed heart failure (InfHF) to those that did not (Inf). Infarct size was similar in both groups. In vitro preparations of tail vascular bed were used to investigate the vascular responses to acetylcholine, sodium nitroprusside and phenylephrine. Acetylcholine - induced relaxation was impaired in the Inf group (53 ± 2 %, n = 6) when compared to Sham (80 ± 2 %, n = 6, p < 0.05). The maximal response (Emax) to phenylephrine increased in the Inf group (423 ± 10 mmHg, n = 9, p < 0.01) and decreased in InfHF (279 ± 10 mmHg, n = 7, p < 0.05) when compared to Sham (319 ± 11 mmHg, n = 8). Regardless of endothelial integrity, Emax to phenylephrine increased in the Inf, L - NAME and indomethacin groups. An increased release of a prostanoid vasodilator was detected in the Inf group. Differently, the InfHF group presented a reduction of the Emax to phenylephrine and an increment of nitric oxide release. This study demonstrates that MI without heart failure impairs endothelium - dependent relaxation and increases the reactivity to phenylephrine. This increase seems to involve a muscular component. The endothelium participates with an increased release of a vasodilator prostanoid, possibly to compensate the increased smooth muscle response. When heart failure follows MI the reactivity to phenylephrine decreases, possibly due to an increased nitric oxide release.


Key words: endothelium, heart failure, myocardial infarction, rat, tail vascular bed, vascular reactivity


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