The influx of 45Ca++ produced by l-norepinephrine (3 X 10(-7) or 10(-5) M) and K+ (100 mM) in rat aorta was not significantly influenced by phenoxybenzamine (1 or 3 X 10(-8) M) present for 5 or 10 min. However, the l-norepinephrine (3 X 10(-7) or 10(-5) M)-mediated 45Ca++ efflux was markedly attenuated by this treatment. Higher concentrations of phenoxybenzamine, as well as extension of the time of exposure, impaired the 45Ca++ influx to l-norepinephrine, but not that to K+. In contrast, prazosin (10(-9)-10(-7) M), as well as N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (10(-7) or 10(-6) M for 5 or 10 min), was equally effective in antagonizing the 45Ca++ in and efflux caused by l-norepinephrine. Exposure of rat aorta to 1.3 X 10(-9) M phenoxybenzamine for 30 min significantly shifted the log concentration-contractile response curve to the full alpha-1 adrenoceptor agonist, l-phenylephrine, to the right and reduced its maximum response but failed to alter the contraction to the partial agonist Sgd 101/75 (indanidine). Conversely, incubations with 2.0, 2.2 and 3.0 X 10(-8) M N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline invariably affected the contractions to Sgd 101/75 more than those to l-phenylephrine. In pithed rats, N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (1 or 2 mg/kg i.v., -30 min), as well as phenoxybenzamine (0.1 mg/kg i.v., -30 min), enhanced the effectiveness of nifedipine to inhibit the vasopressor responses to the alpha-1 adrenoceptor stimulant, cirazoline.(ABSTRACT TRUNCATED AT 250 WORDS)