ALPHA-ADRENOCEPTOR SUBTYPES IN SMOOTH MUSCLES OF RAT PULMONARY-ARTERY

The contributions of subtypes of alpha-adrenoceptor to contraction induced by agonists were studied in smooth muscles of isolated rat pulmonary arteries. The results showed that the antagonizing effects of prazosin on the contraction induced by norepinephrine (NE) or phenylephrine (Phe) were more potent than those of yohimbine. The effect of prazosin against Phe was more potent than against NE, and yohimbine was just the reverse. Preincubation of preparations with chlorethylclonidine (CEC) 50 mumol . L-1, after which only alpha1A adrenoceptors were left, reduced the vascular contraction induced by NE to 36% of the control (P < 0.01). While in the presence of nifedipine 10 mumol . L-1, during which only the responses of alpha1B adrenoceptors were left, the contraction was weakened to 70% (P < 0.05). The pK(A) values of alpha1A subtype (3.37 +/- 0.34) were smaller than those of alpha1B (6.64 +/- 0.40, P < 0.01). But the values of K(A)/EC50 were much higher in alpha1A than those in alpha1B. The results suggest that in smooth muscle of rat pulmonary artery both alpha1 and alpha2 adrenoceptors exist, but alpha1 is superior functionally. Both subtypes of alpha1 adrenoceptor are involved in the contraction induced by NE. Compared with alpha1B subtype, alpha1A subtype has a lower affinity but a more reserve and a higher efficacy for NE.