The effects of thiopental sodium on the adrenergic neuroeffector junction were studied in isolated rabbit pulmonary arteries. Basal tension was not altered by thiopental (2 X 10(-5) and 10(-4) M) but was increased by high concentrations of thiopental (5 X 10(-4) M). Thiopental (10(-4) and 5 X 10(-4) M) potentiated contractions induced by transmural electrical stimulation. Contractile responses to exogenously applied low concentrations of norepinephrine (NE) were potentiated by thiopental (2 X 10(-5), 10(-4) and 5 X 10(-4) M), whereas those to high concentrations were not altered. In strips previously incubated in 1-[7,8-3H]-NE (10(-7) M), the release of [3H] induced by transmural stimulation (5 Hz) was not altered by thiopental (10(-4) and 5 X 10(-4) M). Potentiation by thiopental (10(-4) M) of the responses to transmural stimulation was not affected by prior application of cocaine or hydrocortisone. Contractions induced by alpha receptor agonists (phenylephrine and methoxamine) were potentiated by thiopental (10(-4) M), while those induced by acetylcholine were not altered. Contractile responses to potassium chloride were attenuated by thiopental (10(-4) M). Amobarbital sodium and pentobarbital sodium (10(-4) M, respectively) attenuated contractions induced by NE. It may be concluded that thiopental specifically increases the responsiveness of postsynaptic alpha receptors to NE.