To characterise the pharmacological activity of 2,5-di-t-butyl-1,4-benzohydroquinone (BHQ) on vascular smooth muscle, the different effects of BHQ on rat aorta were investigated under several experimental conditions. In aortic rings at rest or depolarised with 80 mM K+ in the presence of 1 microM nifedipine, BHQ evoked a slow tonic contraction which was antagonised by 1 mM Ni2+. Depolarised rings contracted in response to addition of 1 mM Ca2+, with an EC50 value of 32.4+/-1.0 mM for K+. At 20 mM K+, Ca2+-induced contraction was enhanced by BHQ. This effect was antagonised by 1 mM Ni2+, but not by 1 microM nifedipine. By contrast, at 40, 80 and 128 mM K+, BHQ antagonised Ca2+-induced contraction. This effect was partially reversed by 1 microM methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyri dine-5-carboxylate (Bay K 8644) or by increasing extracellular Ca2+ concentration. In the presence of nifedipine and Ni2+, depolarised rings (80 mM K+) contracted in response to addition of 1 microM phenylephrine; this response was fast and then slowly decreased. When the preparations were preincubated with BHQ, the phenylephrine-induced contraction was transient and antagonised in a concentration-dependent manner by BHQ. These results indicate that the myotonic effect of BHQ on rat aortic rings depends on activation of Ca2+ influx via a Ni2+-sensitive pathway, whereas its myolytic activity is due either to antagonism of Ca2+ entry via L-type Ca2+ channels or depletion of intracellular Ca2+ stores.