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

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Abstract
With pithed normotensive rats we studied the interaction between beta 2-adrenoceptor-mediated vasodilation and pressor responses elicited by vasopressin, the selective alpha 2-adrenoceptor agonists B-HT 920 and UK 14,304, and the alpha 2-adrenoceptor-mediated pressor responses of (--)-norepinephrine, tyramine [via neuronally released (--)-norepinephrine], alpha-methylnorepinephrine, and (--)-epinephrine. Salbutamol was used as a selective agonist of beta 2-adrenoceptors. The selective beta 2-adrenoceptor antagonist ICI 118,551 was employed to reveal the intrinsic beta 2-adrenoceptor activation induced by alpha-methylnorepinephrine and (--)-epinephrine, measured as a potentiation of the increase in diastolic pressure. Two types of interaction between beta 2-adrenoceptor-mediated vasodilation and alpha 2-adrenoceptor-mediated vasoconstriction were found. The effect of the alpha 2-adrenoceptor agonists was attenuated in most cases. However, intravenously administered (--)-norepinephrine elicited an alpha 2-adrenoceptor-mediated vasoconstriction not attenuated by beta 2-adrenoceptor-mediated vasodilation. These results are interpreted as indications for two different populations of vascular alpha 2-adrenoceptors. Neuronally released (--)-norepinephrine activated alpha 2-adrenoceptors, and its effect was attenuated by beta 2-adrenoceptor-mediated vasodilation in contrast to that of intravenously administered (--)-norepinephrine. Therefore, an intrasynaptic and extrasynaptic population of vascular alpha 2-adrenoceptors as postulated. In contrast to (--)-norepinephrine, intravenously administered (--)-epinephrine seems to activate predominantly intrasynaptic alpha 2-adrenoceptors.

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