Contractile responses of bovine retinal microarteries (BRA)(diameter: 198+/-5 microns, n= 49) to beta-antagonists, local anesthetics and Ca2 (+)-antagonists were studied in vitro. Propranolol (10 (-8)-10 (-5) M) relaxed K (+)-activated BRA dose-dependently, whereas timolol (10 (-8)-10 (-5) M) relaxed K (+)-activated BRA only weakly at the highest doses. The relaxation by propranolol was not mediated through interaction with adrenergic nerve endings, since fluorescence histochemistry showed absence of such nerve endings in BRA. In addition, propranolol still relaxed BRA which were treated with 6-hydroxydopamine (6-OHDA), which causes chemical adrenergic denervation. Local anesthetic properties of propranolol had no part in the relaxation: lidocaine (10 (-7)-10 (-5) M) did not relax K (+)-activated BRA. Verapamil (10 (-9)-10 (-6) M) relaxed K (+)-activated BRA markedly and dose-dependently. Both verapamil and propranolol relaxed phasic K (+)-induced force more than tonic force. By contrast, they relaxed only the tonic part of serotonin-induced force, and they had no effect on stretch-induced active force. Therefore: 1) propranolol dilates BRA more than does timolol, possibly because of the Ca2 (+)-antagonistic properties of the former; 2) beta-and Ca2 (+)-antagonists probably spare myogenic autoregulation of blood flow and do not prevent, but could partially reverse, serotonin-induced arterial spasm.