All [beta]-adrenergic antagonists have an asymmetric carbon atom, and most commercially available [beta]-blockers consist of (R)-and (S)-enantiomers in a fixed 1: 1-ratio. The drugs are believed to be contraindicated when peripheral vascular disease exists, presumably due to unopposed adrenergic vasoconstriction. However, little is known about direct vascular effects of [beta]-blockers or of Stereoselective effects on peripheral arteries. Therefore, we investigated the effects on forearm blood flow (FBF) of brachial artery infusions of the (R)-and (S)-enantiomers of propranolol and atenolol (2, 10, and 50 [mu] g/min each) and their inhibitory effects on isoprenaline (Iso)-induced vasodilatation by forearm venous occlusion plethysmography in 12 healthy subjects. Only (R)-propranolol caused an increase in FBF (+ 21%, p< 0.05), whereas (S)-propranolol and (R)-and (S)-atenolol had no direct effect on peripheral arteries. Vasodilatation induced by Iso was abolished by (S)-propranolol and reduced by (R)-propranolol (-56%, p< 0.05) and (5)-atenolol (-68%, p< 0.05), whereas (R)-atenolol had no effect. Our results indicate that the optically pure (R)-and (S)-enantiomers of propranolol and atenolol do not exert direct vasoconstrictive effects. Furthermore, our results confirm that predominantly (S)-enantiomers have [beta]-adre-noceptor blocking effects, but they also show that neither the non-[beta]-blocking (R)-enantiomer of propranolol nor the (S)-enantiomer of the [beta] 1-selective agent atenolol is completely devoid of blocking effects on vascular [beta] 2-adrenoceptors.