Vascular Ó1D-Adrenoceptor function is maintained during congestive heart failure after myocardial infarction in the rat

RESUMO

Background. During congestive heart failure, desensitization of ß-adrenoceptors is related to a lower adrenergic responsiveness in the heart; little is known about Ó1D-adrenoceptors in the vasculature under this condition. We evaluated Ó1D-adrenoceptor response in aorta and carotid arteries in a model of congestive heart failure (CHF) post-myocardial infarction. Methods. Noradrenaline-elicited contraction was determined in endothelium-denuded arterial rigs from young (10-week-old) Wistar rats in the absence and presence of the Ó1D-adrenoceptor antagonist BMY 7378 (8-(2-(4-(2-methoxyphenyl)-1-piperazinyl) ethyl)-8-azaspiro(4,5)decane-7,9-dione dihydrochloride) in sham-operated rats and in rats that development CHF 4 weeks or 7 months after myocardial infarction. Results. In the thoracic aorta, BMY 7378 displaced noradrenaline affect to the right with PA2 values of sham, 8.58 ñ 0.12; CHF, 8.36 ñ 0.13, and sham, 8.50 ñ 0.10; CHF, 7.99 ñ 0.13 at 4 weeks and 7 months after myocardial infarction, respectively. While in carotid arteries, the pA2 values were sham, 8.43 ñ 0.19; CHF, 8,81 ñ 0.19, and sham, 8.35 ñ 0.18; CHF, 8,29 ñ 0.08 at 4 weeks and 7 months after myocardial infarction, respectively. Ehen adul (7-month-old) rats were subjected to myocardial infarction, CHF was not installed and pA2 values were similar and high in both sham and infarcted rats. Conclusions. These results indicate that Ó1D-adrenoceptors remained as the main receptors involved in contraction in aorta and carotid arteries, irrespective of CHF duration