Abstract

AbstractPurpose: There is clinical evidence suggesting that the neurotransmitter dopamine may play a role in regulating retinal vascular function. Patients with Parkinson's disease tend to have a narrower retinal vessel diameter in fundus images and reduced perfusion density1. Healthy volunteers given dopamine IV show increased retinal blood cell velocity (by 37%) and fundus pulsation amplitude (by 24%)2. However, it is not clear if these observed effects may be due to direct actions of dopamine on retinal vessels, independent of any systemic actions, and if so through which subtype of dopamine receptors. We therefore measured the effects of dopamine ligands on isolated segments of porcine retinal arterioles by small wire myography.Methods: Dissected segments of porcine retinal arterioles and surrounding retinal tissue were mounted in a DMT630MA small wire myograph system for measurement of contractile activity, and pre‐contracted with 10−6 MU‐46619, a thromboxane analog, added to the organ bath. With the vascular tone stabilized, all dopamine ligands tested were applied separately to the bath with the vessel, and the effects of each on the wall tension recorded. Results are presented as wall tension (in mN/mm) normalized for vessel length.Results: In isolated vessel segments pre‐contracted with U‐46619, dopamine induced a vasodilation in a dose‐dependent manner, which was complete at 2 mM. The dopamine D1 receptor agonist SKF38393 induced dose‐dependent vasodilation, complete at 0.7 mM. The D2 receptor agonist sumanirole (10−4 M) had no effect on wall tension in pre‐contracted retinal arterioles. The D2 receptor antagonist S‐sulpiride (10−3 M) had no effect on wall tension and did not block the vasodilation induced by either dopamine or SKF38393.Conclusions: Dopamine induces vasodilation in pre‐contracted retinal arterioles, primarily via D1 receptors.

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