Interaction Between β2-Adrenoceptor-Mediated Vasodilation and α1-Adrenoceptor-Mediated Vasoconstriction in the Pithed Normotensive Rat

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Abstract
With pithed normotensive rats we studied the interaction between β2-adrenoceptor-mediated vasodilation and α1-adrenoceptor-mediated vasoconstriction. The selective β2-adrenoceptor agonist salbutamol was used to elicit vasodilatation. To induce α1-adrenoceptor-mediated vasoconstriction, the selective α1-adrenoceptor agonists cirazoline, St 587, and methoxamine were used. Furthermore, the α1-adrenoceptor-mediated vasopressor effects of intravenously administered (—)-norepinephrine, and (—)-norepinephrine released from neurons by the nicotinic agonist 1,1-dimethyl-4-phenylpiperazine iodide (DMPP), the muscarinic ganglionic stimulant McN-A-343, electrical stimulation of the spinal cord, and the indirect sympathomimetic agent tyramine, were studied. By using the selective β2-adrenoceptor antagonist ICI 118.551, the interaction between the α1-adrenoceptor-mediated vasoconstriction of (—)-epinephrine and α-methylnorepinephrine with their intrinsic β2-adrenoceptor agonistic effects was investigated. Two types of interaction between α1- and β2-adrenoceptor-mediated vascular effects were found. Cirazoline and McN-A-343 activated α1-adrenoceptors, inducing a vasoconstriction not affected by β2-adrenoceptor-mediated vasodilation. However, methoxamine at low doses, St 587, DMPP, electrical stimulation, intravenously administered (—)-norepinephrine, (—)-epinephrine, and α-methylnorepinephrine activated α1-adrenoceptors, and their effect was attenuated by vasodilation. At low doses, tyramine stimulated α1-adrenoceptors that were not sensitive to β2-adrenoceptor-mediated vasodilation, in contrast to the population of α1-adrenoceptors activated at high doses of tyramine. It is hypothesized that there exist two different populations of α1-adrenoceptors.

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