Effects of terbutaline applied in vivo or in vitro on alpha-adrenergic receptors in the rabbit aorta in normal and Ca(2+)-free solution, and on basal, high potassium-, and phenylephrine-stimulated Ca2+ uptake into aorta were investigated. Three day terbutaline administration (25 mg/kg, subcutaneously three times daily) to rabbits increased the pKB for phentolamine in aorta rings (control 7.3 +/- 0.2, n = 9; terbutaline 7.8 +/- 0.2, n = 15). It also depressed phenylephrine-stimulated contractions of aorta rings in Ca(2+)-free but not those in normal Krebs solution. It did not significantly depress the basal, or phenylephrine-evoked Ca2+ influx into aorta rings, but decreased high potassium-induced Ca(2+)-influx (control 0.58 +/- 0.05 mumoles/g aorta; n = 3, terbutaline 0.41 +/- 0.06 mumoles/g aorta, n = 3). In vitro application of 50 microM terbutaline did not significantly alter phenylephrine-stimulated contractions of aorta rings in Ca(2+)-free Krebs solution or significantly depress basal or phenylephrine-induced Ca2+ influx into aortas, but did decrease high potassium-stimulated Ca(2+)-influx. Thus, 3-day terbutaline administration increased the affinity of alpha-adrenergic receptors for phentolamine and had a tendency to increase contractions of aorta rings to phenylephrine. It also decreased high potassium-stimulated Ca2+ influx, and depressed phenylephrine-induced contractions in Ca(2+)-free Krebs solution, while in vitro terbutaline application also decreased potassium-induced Ca2+ influx.