BETA-1 AND BETA-2 ADRENOCEPTOR-MEDIATED RESPONSES IN PREPARATIONS OF PULMONARY-ARTERY AND AORTA FROM YOUNG AND AGED RATS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 228  (3) , 733-738
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 ICI 118,551 [corwin] (.beta.2 selective) indicated that the minor population (.beta.1) was less important in aorta than in pulmonary artery. On preparations from 18-mo.-old rats, the maximum relaxation to isoproterenol (20.4%, aorta and 67.9%, pulmonary atery) 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. The negative log EC50 [median effective concentration] of fenoterol, but not of isoproterenol of norepinephrine, was less than in preparations from young rats. This could indicate that aging had affected .beta.2 more than .beta.1 adrenoceptor-mediated respones and may explain why aging depressed the maximum relaxation of aorta more than that of pulmonary artery.

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