| Abstract: | Rat pulmonary artery contains both alpha adrenoceptors mediating contraction and beta-1 and beta-2 adrenoceptors mediating relaxation. Neither alpha nor beta adrenoceptor-mediated responses of this vessel to norepinephrine or epinephrine were potentiated by cocaine, despite evidence for the presence of some adrenergic nerves. Beta adrenoceptor-mediated relaxation of pulmonary artery, but not aorta, modulated alpha adrenoceptor-mediated contractions to epinephrine but not norepinephrine. Rat aorta also contains both beta-1 and beta-2 adrenoceptors mediating relaxation, in that Schild plots for atenolol (beta-1 selective antagonist) using a beta-1 selective agonist (norepinephrine) and a beta-2 selective agonist (fenoterol), respectively, were not superimposed. The Schild plot data for lCl 118,551 (beta-2 selective) indicated that the minor population (beta-1) was less important in aorta than in pulmonary artery. On preparations from 18-month-old rats, the maximum relaxation to isoproterenol (20.4%, aorta and 67.9%, pulmonary artery) was less than in preparations from young rats (79.8%, aorta and 96.9%, pulmonary artery), i.e., aging had reduced the beta adrenoceptor-mediated relaxation in both vessels, but particularly in aorta. Also, the negative log EC50 of fenoterol, but not of isoproterenol or norepinephrine, was less than in preparations from young rats. This could indicate that aging had affected beta-2 more than beta-1 adrenoceptor-mediated responses and may explain why aging depressed the maximum relaxation of aorta more than that of pulmonary artery. |
