Influence of ephedrine and the role of alpha subtype adrenoreceptors in the vascular bed of the cat lung.

In a university research laboratory and in separate experiments, the effects of phentolamine, the alpha-adrenergic antagonist; prazosin, an alpha1-adrenoceptor antagonist; 5-methyl-urapidil, the selective alpha1A-subtype adrenoceptor antagonist; chloroethylclonidine, an alpha1B- and alpha1D-subtype adrenoceptor antagonist; and BMY 7378, a selective alpha1D-subtype adrenoceptor antagonist were analyzed in an attempt to identify any significant effect on pulmonary arterial responses to ephedrine and other agonist agents in the pulmonary vascular bed of the cat. Under constant flow conditions, lobar arterial perfusion pressure and systemic pressure were continuously monitored, electronically averaged, and permanently recorded. In the isolated left lower lobe of the pulmonary feline vascular bed, ephedrine induced a dose-dependent vasoconstrictor response that was not significantly altered following administration of 5-methyl-urapidil. The vasopressor activity as a result of ephedrine was significantly decreased after administration of phentolamine, prazosin, chloroethylclonidine, and BMY 7378. Further, when the alpha1B- and alpha1D-subtype adrenoceptor antagonist chloroethylclonidine was given, there was almost complete elimination of the ephedrine-induced vasoconstrictor response. The results of this study suggest that ephedrine causes a dose-dependent vasopressor response in the feline pulmonary vascular bed and that this activity may be mediated or modulated by both alpha1B- and alpha1D-subtype adrenoceptor sensitive pathways.