Sympathetic vasodilation in the rat anterior choroid mediated by beta(1)-adrenoceptors

Electrical stimulation of the preganglionic superior cervical nerve produced a frequency-dependent vasoconstrictor response in the anterior choroidal blood vessels of the eye of anesthetized rats. Systemic administration of phentolamine (5 mg kg(-1)) reversed the vasoconstriction to a vasodilator response. This sympathetic-evoked vasodilation was not antagonized by inhibition of nitric oxide synthase with N(G)-nitro-L-arginine methyl ester (L-NAME) (20 mg kg(-1)) or by inhibition of cyclo-oxygenase with indomethacin (20 mg kg(-1)). Intravenous administration of propranolol (1 mg kg(-1)), as well as selective beta(1)-adrenoceptor antagonists atenolol (3 mg kg(-1)), timolol (0.3 mg kg(-1)), and betaxolol (0.1 mg kg(-1)), totally abolished the sympathetic nerve evoked ocular vasodilation. In contrast, the selective beta(2)-adrenoceptor antagonist, ICI-118, 551 ((+/-)-1-[2, 3-(Dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2- butanol) (0.3 mg kg(-1), i.v.), was without effect. These results support the conclusion that the residual sympathetic ocular vasodilation observed in the rat anterior choroid after alpha-adrenoceptor blockade is mediated exclusively by neurogenic release of norepinephrine acting on vascular beta(1)-adrenoceptors.