Dopaminergic vasodilation in the choroidal circulation by d1/d5 receptor activation

To test whether exogenous dopamine can cause choroidal vasodilation and to identify the mediating receptors in anesthetized rabbits.

Mean arterial pressure (MAP), intraocular pressure (IOP), and orbital venous pressure (OVP) were measured by direct cannulation of the central ear artery, the vitreous, and the orbital venous sinus, respectively. Laser Doppler flowmetry was used to measure choroidal blood flow (ChorBF) while MAP was manipulated mechanically with occluders on the aorta and vena cava, thus changing perfusion pressure (PP) over a wide range. In the first group of animals (n = 11), pressure-flow (PF) relationships were performed at control and in response to 40 micro g/kg per minute intravenous (IV) dopamine (D40) and D40+SCH-23390 (0.5 mg/kg, bolus injection IV). In the second group of animals (n = 6), PF relationships were recorded at control and during infusion of SKF-38393 (80 micro g/kg per minute).

D40 lowered IOP and caused an upward shift in the choroidal PF relationship, which was blocked by the D1/D5 antagonist SCH-23390 suggesting the involvement of the dopamine D1/D5 receptors. Stimulation of the D1/D5 receptors by infusion of the selective agonist SKF-38393 also lowered IOP and caused an upward shift in the PF relationship. Dopamine and SKF-38393 tended to decrease OVP, but the effect was not significant.

Dopamine can cause choroidal vasodilation in anesthetized rabbits. Because SCH-23390 was able to block the response and SKF-38393 caused a similar vasodilation, we conclude that the vasodilation is caused by a D1/D5-receptor-mediated mechanism.