AN INVESTIGATION INTO THE POSSIBLE PHYSIOLOGICAL ROLES OF VASCULAR α1- AND α2-ADRENORECEPTORS

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Abstract
The influence of chemical sympathectomy or bilateral adrenal demedullation on vasopressor responses produced by the .alpha.1-adrenoreceptor agonist, phenylephrine, and the .alpha.2-adrenoreceptor agonist, M-7 [2-N,N-dimethylamino-5,6-dihydroxy-1,2,3,4-tetrahydronaphthalene], was investigated in pithed rats to see if either procedure induced selective supersensitivity to either of these compounds. 5-HT [5-hydroxytryptamine], a tryptaminergic vasopressor agent, was also used to discriminate between non-specific changes in vascular responsiveness and those mediated via .alpha.-adrenoreceptors. Adrenal demedullation caused a slight reduction in the sensitivity to all agonists. Chemical sympathectomy reduced the vasopressor responses to all doses of phenylephrine, but responses to 5-HT were unchanged. Responses to M-7 tended to be greater in sympathectomized rats than in untreated rats. Circulating adrenal medullary catecholamines apparently do not physiologically modulate vascular .alpha.-adrenoreceptor function. The differential effect of chemical sympathectomy on the vasopressor responses to phenylephrine and M-7 might be explained in terms of a small increase in the ratio of vascular .alpha.2:.alpha.1-adrenoreceptors, that receive a noradrenergic innervation.

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