Vascular α1D-Adrenoceptor Function is Maintained During Congestive Heart Failure After Myocardial Infarction in the Rat

Background congestive heart failure, desensitization of β-adrenoceptors is related to a lower adrenergic responsiveness in the heart; little is known about α1-adrenoceptors in the vasculature under this condition. We evaluated α1D-adrenoceptor response in aorta and carotid arteries in a model of congestive heart failure (CHF) post-myocardial infarction. s enaline-elicited contraction was determined in endothelium-denuded arterial rings from young (10-week-old) Wistar rats in the absence and presence of the α1D-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 developed CHF 4 weeks or 7 months after myocardial infarction. s thoracic aorta, BMY 7378 displaced noradrenaline effect to the right with pA2 values of: sham, 8.58 ± 0.12; CHF, 8.36 ± 0.13, and sham, 8.56 ± 0.10; CHF, 7.99 ± 0.13 at 4 weeks and 7 months after myocardial infarction, respectively. While in carotid arteries, the pA2 values were: sham, 8.43 ± 0.19; CHF, 8.81 ± 0.19, and sham, 8.35 ± 0.18; CHF, 8.29 ± 0.08 at 4 weeks and 7 months after myocardial infarction, respectively. When adult (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. sions results indicate that α1D-adrenoceptors remained as the main receptors involved in contraction in aorta and carotid arteries, irrespective of CHF duration.