Impaired retinal vasodilator response to acetylcholine in a rat model of NMDA-induced retinal degeneration.

Previous studies have shown that degeneration of retinal capillaries occurs following N-methyl-D-aspartate (NMDA)-induced retinal neurotoxicity, but it is unclear whether vasodilatory mechanisms are altered in retinal blood vessels. The purpose of the present study was to determine whether retinal vasodilator responses are affected in a rat model of NMDA-induced retinal damage. At 14 days after a single intravitreal injection of NMDA (200 nmol), retinal vasodilator responses were assessed by measuring the diameter of retinal arterioles in fundus images.

Noradrenaline contracts rat retinal arterioles via stimulation of α(1A)- and α(1D)-adrenoceptors.

The aim of this study was to characterize the α₁-adrenoceptor subtype(s) involved in the noradrenaline-induced contraction of retinal arterioles in rats. In vivo ocular fundus images were captured with a digital camera equipped with a special objective lens. By measuring changes in diameter of retinal arterioles in the fundus images, retinal vascular response was assessed.

Hyperglycemia accelerates impairment of vasodilator responses to acetylcholine of retinal blood vessels in rats.

We previously reported that vascular endothelial functions in both retinal and systemic circulation are impaired 6-8 weeks after induction of hyperglycemia with streptozotocin (STZ) in rats. However, it remains to be elucidated whether the period required for the onset of endothelial dysfunction is different, depending on vascular beds and severity of hyperglycemia. In this study, we examined the effects of several vasodilators on the diameter of retinal blood vessel and blood pressure in Control, STZ (STZ treatment alone), and STZ+Glc (STZ treatment plus D-glucose feeding) rats.