In the rabbit isolated thoracic aorta, WB 4101 and 5-methylurapidil dose-dependently shifted the concentration-response curves for norepinephrine to the right. Schild plots showed that the inhibition of responses for WB 4101 and 5-methylurapidil was biphasic, implying that norepinephrine acted through two receptor populations. Clonidine produced a concentration-dependent contraction in the isolated rabbit thoracic aorta. WB 4101 and 5-methylurapidil antagonized the contractions for cloni dine, and the Schild plot to both antagonists against clonidine yielded a monophasic slope. Schild plots of the results obtained from the inhibition by WB 4101 and 5-methylurapidil for norepinephrine in strips pretreated with chloroethylclonidine yielded a straight line with a slope of unity. Specific binding of [3H]prazosin in the aortic membrane preparations was saturable. The Hill coefficient obtained from the inhibition curves for clonidine was significantly different from unity. Clonidine interacted with two binding sites labelled by [3H]prazosin, but the low affinity site was completely eliminated by pretreat ment with 10,uM chloroethylclonidine. These results suggest that the subtype activated by nor epinephrine is different from that activated by clonidine, and that norepinephrine-induced contraction through both a IA and a ,B-subtypes and clonidine through only the a IA-subtype in the rabbit thoracic aorta.
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