title: Vascular alpha 1D-adrenoceptor function is maintained during congestive heart failure after myocardial infarction in the rat.
abstract: 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.
authors.affiliation: Facultad de Estudios Superiores-Cuautitlán, Universidad Nacional Autónoma de México, D.F., Mexico.
authors.forename: L
authors.initials: L
authors.lastname: Martínez
authors.forename: L
authors.initials: L
authors.lastname: Carmona
authors.forename: R
authors.initials: R
authors.lastname: Villalobos-Molina
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000503:physiopathology; D001835:Body Weight; D002339:Carotid Arteries / Q000187:drug effects / Q000503:physiopathology; D004195:Disease Models, Animal; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology*; D006439:Hemodynamics; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009638:Norepinephrine / Q000494:pharmacology; D009929:Organ Size; D010879:Piperazines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D010879:Piperazines; D018340:Receptors, Adrenergic, alpha-1; D014662:Vasoconstrictor Agents; C053428:BMY 7378; D009638:Norepinephrine