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H. A. Reitsamer, H. Brandtner, C. Runge, B. Bogner, C. Strohmaier, F. Taher, G. Grabner, F. Schroedl; VIP, PACAP and Nitric Oxide Interaction in Choroidal Blood Flow Regulation. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3446.
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To investigate the role of VIP, PACAP and NO and their interaction in the regulation of choroidal blood flow in rabbits.
In anesthetized New Zealand White rabbits (n=12) mean arterial pressure (MAP) and intraocular pressure (IOP) were measured by direct cannulation of the central ear artery and the vitreous respectively. Laser Doppler flowmetry was used to measure choroidal blood flow (ChorBF) continuously 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 i.v. administration of VIP (20 ng/kg/min), PACAP-27 (10 ng/kg/min), non selective competitive antagonists VIP6-28 (80ng/kg, bolus), PACAP6-38 (20µg/kg, bolus) to their receptors and the non selective NOS inhibitor L-NAME (128 mg/kg, bolus).
VIP caused a maximum increase of ChorBF by 109±18% and a 54±4% decrease in ChorR, while PACAP caused an comparable increase of 86±18% in ChorBF and 46±6% decrease in ChorR. On average the receptor antagonists blocked roughly 62±15% of the total effect (n=5). L-NAME blocked the rest of the effect (n=5).
VIP and PACAP are highly effective vasodilators in the posterior choroid. A large part of their vasodilatory action can be blocked by L-NAME, however there is also a nitric oxide independently mediated part of the blood flow response to these two neuropeptides which can be blocked by receptor antagonists for VIP and PACAP respectively. However, the percentage of effect that can be blocked seems to be dependent on the infusion rate of the neuropeptide, which might be due to the competitive nature of the antagonists.
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