Purpose:
It was shown previously that exogenous dopamine causes choroidal vasodilation via D1/D5 receptor mediated mechanisms (Invest Ophthalmol Vis Sci. 2004 Mar;45(3):900–5). In the present study we investigate the role of D1/D5 receptor activation by endogenous dopamine.
Methods:
In anesthetized New Zealand rabbits (n=11) 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 placed around the aorta and vena cava, thus changing ocular perfusion pressure (PP) over a wide range. Pressure–flow (PF) relationships were measured at control and in response to the dopamine D1/D5 receptor blocker SCH23390 (0.5mg/kg, bolus injection i.v.).
Results:
The D1/D5–antagonist SCH23390 significantly decreased IOP and ChorBF whereas choroidal resistance (ChorR) and OVP were increased. D1/D5 receptor blockage had no significant effect on MAP, PP and HR (heart rate). The pressure flow relationship was shifted downwards significantly. The baseline results are summarized in the table. . Baseline effects of SCH–23390
Conclusions:
The results of this study indicate the presence of endogenous dopaminergic activity in the choroid contributing to the basic vasodilatory tone in the choroid via a D1/D5 receptor mediated mechanism.
Keywords: dopamine • choroid • blood supply