Subtypes of α₁-Adrenoceptors Involved in Noradrenaline-Induced Contractions of Rat Thoracic Aorta and Dog Carotid Artery

Abstract

We tried to determine α₁-adrenoceptor subtypes involved in noradrenaline-induced contractions of rat thoracic aorta and dog carotid artery. Prazosin competitively antagonized the contractions induced by noradrenaline in both the arteries with a high pK_B value (approximately 9.7). WB4101, benoxathian, phentolamine, HV723 and 5-methylurapidil also competitively antagonized the responses to noradrenaline in both the arteries: however, the affinities for the antagonists were significantly higher in the rat thoracic aorta than in the dog carotid artery. The affinities for the competitive antagonists were not changed by treatment with nifedipine. In the rat thoracic aorta, chlorethylclonidine (CEC) elicited either a persistent contraction with rhythmic activities before treatment with nifedipine or partial inactivation of α₁-adrenoceptors in the presence of nifedipine. On the other hand, CEC produced only inactivation of α₁-adrenoceptors in the dog carotid artery. These results suggest that noradrenaline-induced contractions of the rat thoracic aorta and dog carotid artery are respectively mediated through distinct α₁-adrenoceptor subtypes. According to the α_1A, α_1B subclassification, the α₁-adrenoceptor of dog carotid artery is like the α_1B subtype, while that of rat thoracic aorta is atypical. Both subtypes are also identified as a high affinity site for prazosin (α_1H subtype) in the α_1H, α_1L and α_1N subclassification.