Contractions were induced in rings of rabbit pulmonary artery with the preferential α1-adrenoceptor agonists, whereas St 587, clonidine and B-HT 920 were (parchloro-trifluoromethyl-phenylimino)[imidazolidine] and the preferential α2-adrenoceptor agonists, clonidine and B-HT 920 [6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-(4,5-d) azepine]. Phenylephrine and methoxamine acted as full agonists whereas St 587, clonidine and B-HT 920 were partial agonists (intrinsic activities 0.62, 0.38 and 0.42, respectively). Experiments with α1- and α2-adrenoceptor antagonists indicated that the receptors involved are of the α1 type only. Removal of extracellular Ca2+ inhibited maximal contractions to phenylephrine and methoxamine by 30% and 49%, respectively. The remaining contraction components of the full agonists were abolished by the “intracellular Ca2+ antagonist” TMB-8 [8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate]. Contractions to St 587, clonidine and B-HT 920 were virtually abolished in Ca2+-free medium. Pretreatment of the donor rabbits with pertussis toxin (2.5 μ/kg i. v., 5–6 days before sacrifice) attenuated the efficacies of the full agonists, phenylephrine and methoxamine by only 24% and 17%, respectively, whereas maximal contractions to the partial agonists, St 587, clonidine and B-HT 920, were inhibited by 46%, 61% and 75%, respectively. Also the sulfhydryl reagent, N-ethylmaleimide (10 μM), reduced contractile efficacies of phenylephrine and methoxamine to a lesser degree than those of St 587, clonidine and B-HT 920. When agonists were used at equieffective concentrations (i.e. EC30–40 for phenylephrine and methoxamine, EC70–80 for St 587 and EC99 for clonidine and B-HT 920) the degree of inhibition by removal of extracellular Ca2+, pertussis toxin and N-ethylmaleimide was similar for all agonists. These data suggest that a unitary al-receptor may stimulate contractions via two different mechanisms. At a low degree of receptor stimulation, contractions are mediated by a pertussis toxin- and N-ethylmaleimide-sensitive influx of external Ca2+. At a higher degree of receptor stimulation, an additional mechanism is activated which is insensitive to the two G protein inhibitors and mediated by Ca2+ mobilization from intracellular sites.