Interaction Between β2-Adrenoceptor-Mediated Vasodilation and α2-Adrenoceptor-Mediated Vasoconstriction in the Pithed Normotensive Rat

With pithed normotensive rats we studied the interaction between β2-adrenoceptor-mediated vasodilation and pressor responses elicited by vasopressin, the selective α2-adrenoceptor agonists B-HT 920 and UK 14,304, and the α2-adrenoceptor-mediated pressor responses of (−)-norepinephrine, tyramine [via neuronally released (−)-norepinephrine], α-methylnorepinephrine, and (−)-epinephrine. Salbutamol was used as a selective agonist of β2-adrenoceptors. The selective β2-adrenoceptor antagonist ICI 118.551 was employed to reveal the intrinsic β2-adrenoceptor activation induced by α-methylnorepinephrine and (−)-epinephrine, measured as a potentiation of the increase in diastolic pressure. Two types of interaction between β2-adrenoceptor-mediated vasodilation and α2-adrenoceptor-mediated vasoconstriction were found. The effect of the α2-adrenoceptor agonists was attenuated in most cases. However, intravenously administered (−)-norepinephrine elicited an α2-adrenoceptor-mediated vasoconstriction not attenuated by β2-adrenoceptor-mediated vasodilation. These results are interpreted as indications for two different populations of vascular α2-adrenoceptors. Neuronally released (−)-norepinephrine activated α2-adrenoceptors, and its effect was attenuated by β2-adrenoceptor-mediated vasodilation in contrast to that of intravenously administered (−)-norepinephrine. Therefore, an intrasynaptic and extrasynaptic population of vascular α2-adrenoceptors is postulated. In contrast to (−)-norepinephrine, intravenously administered (−)-epinephrine seems to activate predominantly intrasynaptic α2-adrenoceptors.