The two subtypes of alpha 1-adrenoceptors in blood vessels were compared between stroke prone spontaneously hypertensive rats (SHRSP) and WKY rats in vitro and in vivo. Pretreatment with 50 mumol/L chlorethylclonidine (CEC) for 30 min decreased the maximal contractions induced by norepinephrine (NE) to 31.4 +/- 8.3% and 35.2 +/- 2.9% (aortae); 68.4 +/- 8.2% and 80.1 +/- 7.2% (renal arteries); 68.4 +/- 6.3% and 5.4 +/- 7.0% (mesenteric arteries) of the controls in the SHRSP and the WKY rats, respectively. All the differences between the SHRSP and WKY rats were not statistically significant. In contrast, the blocking effects of nifedipine were much stronger in the SHRSP rats than those in the WKY rats. In the presence of 10 mumol/L nifedipine the maximal contractions induced by NE were decreased to 3.1 +/- 1.5% and 56.5 +/- 4.8% (P < 0.01, aortae); 9.0 +/- 4.1% and 23.6 +/- 3.5% (P < 0.05, renal arteries); 5.9 +/- 2.5% and 28.0 +/- 0.8% (P < 0.01, mesenteric arteries) of the controls in the SHRSP and the WKY rats, respectively. The experiment in vivo also showed that the effects of nifedipine on decreasing basal blood pressure and on antagonizing phenylephrine were increased in the SHRSP rats, as compared to the WKY rats. Analyses of two components of the contractions induced by 10 mumol/L NE in aortae demonstrated that both phasic and tonic contractions were mainly caused by activations of the alpha 1B subtype. There were no significant differences of blocking effects of nifedipine on the phasic contractions between the SHRSP and WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)