Ma huang and alpha subtype adrenoceptors in the cat pulmonary vascular bed

To test the hypothesis that ma huang induces a pressor response in the pulmonary vascular bed of the cat and identify the alpha (1)-adrenoceptor subtype pathway(s) involved in the mediation or modulation of these effects.

Prospective vehicle controlled study.

University research laboratory.

Intact chest preparation; adult mongrel cats.

In separate experiments, the effects of phentolamine, the alpha-adrenergic antagonist; prazosin, a selective alpha (1)-adrenoceptor antagonist; BMY 7378, a selective alpha (1) D-subtype adrenoceptor antagonist; 5-methyl-urapidil, the selective alpha (1)A-subtype adrenoceptor antagonist; and chloroethylclonidine, an alpha (1)B-subtype and (1) D-subtype adrenoceptor antagonist, were investigated on pulmonary arterial responses to ma huang 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 feline vascular bed of the isolated left lower lobe, ma huang induced a dose-dependent vasopressor response that was not significantly attenuated following administration of 5-methyl-urapidil. However, the responses to Ma huang were significantly reduced after administration of phentolamine, prazosin, BMY 7378, and chloroethylclonidine.

The results of the present study suggest that ma huang has potent vasopressor activity in the pulmonary vascular bed of the cat and that this response may be mediated or modulated by both alpha (1)B-subtype and (1)D-subtype adrenoceptor sensitive pathways.