Stimulation of β1- and β2-adrenoceptors dilates retinal blood vessels in rats

Abstract

Our previous studies have demonstrated that adrenaline dilates rat retinal arterioles by stimulating propranolol-sensitive β-adrenoceptors and β3-adrenoceptors, and selective stimulation of β2- or β3-adrenoceptors causes retinal vasodilator responses. In the present study, we compared the effects of β1- and β2-adrenoceptor stimulation on rat retinal arterioles in vivo. Rat ocular fundus images were captured using an original high-resolution digital fundus camera. Diameters of retinal arterioles contained in the images were measured. Systemic blood pressure and heart rate were recorded continuously. Denopamine, a β1-adrenoceptor agonist, increased the diameter of retinal arterioles and heart rate, and produced a small but statistically insignificant decrease in mean arterial pressure. CGP20712A, a β1-adrenoceptor antagonist, but not ICI118551, a β2-adrenoceptor antagonist, significantly prevented denopamine-induced retinal vasodilator and heart rate responses. Salbutamol, a β2-adrenoceptor agonist, increased the diameter of retinal arterioles and decreased mean arterial pressure without significantly changing heart rate. The effects of salbutamol were significantly prevented by ICI118551, but not by CGP20712A. These results suggest that stimulation of β1- and β2-adrenoceptors dilates retinal blood vessels and indicate that all three β-adrenoceptor subtypes (β1, β2, and β3) may be involved in the retinal vasodilator response to adrenaline in rats.