Vascular alpha 1D-adrenoceptor function is maintained during congestive heart failure after myocardial infarction in the rat.
Klíčová slova
Abstraktní
BACKGROUND
During congestive heart failure, desensitization of beta-adrenoceptors is related to a lower adrenergic responsiveness in the heart; little is known about alpha 1-adrenoceptors in the vasculature under this condition. We evaluated alpha 1D-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 rings from young (10-week-old) Wistar rats in the absence and presence of the alpha 1D-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.
RESULTS
In the 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.
CONCLUSIONS
These results indicate that alpha 1D-adrenoceptors remained as the main receptors involved in contraction in aorta and carotid arteries, irrespective of CHF duration.
