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Barbara Bogner, Christian W. Runge, Clemens A. Strohmaier, Falk Schroedl, Andrea Trost, Herwig Brandtner, Günther Grabner, Herbert A. Reitsamer; The Effect of Vasopressin-Antagonists on Choroidal and Ciliary Blood Flow. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6031.
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In-vivo studies have shown that Vasopressin (AVP) is a highly potent vasoconstrictor in the eye (ARVO E-Abstract 359, 2008). Immunohistochemistry proved the presence of V1- and V2-receptors in choroidal and ciliary blood vessels. The aim of this study is the functional characterization of the vasopressin-receptor subtypes involved in blood flow regulation in the choroidal and ciliary vascular bed in the acute rabbit model.
In anesthetized rabbits (n = 6) 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. To change the perfusion pressure (PP) over a wide range, MAP was manipulated mechanically via occluders placed around the aorta and the inferior vena cava. Laser Doppler flowmetry was used to record choroidal blood flow (ChorBF) and ciliary blood flow (CilBF) continuously. To induce vasoconstriction after baseline measurements arginine-vasopressin (AVP) (infusion rate: 1,3 ng/kg/min) was applied intravenously. A V1-receptor antagonist ([β-Mercapto-β,β-cyclopentamethylenepropionyl1, O-me-Tyr2, Arg8]-Vasopressin) and a V2-receptor antagonist ([Adamantaneacetyl1, O-Et-D-Tyr2, Val4, Aminobutyryl6, Arg8,9]-Vasopressin) were given by intravenous bolus injection.
The vasoconstrictive response to AVP caused a 20% reduction of ChorBF, which could be blocked by the V1-receptor antagonist (p < 0.001), whereas the administration of the V2-receptor antagonist had no effect (n. s.). In the ciliary body the AVP-induced vasocostriction was slightly higher than in the choroid. Nevertheless, the response to the applied antagonists resembles that of the choroid.
Although V1 and V2-receptors are both expressed in ocular vessels, the functional data suggest that the AVP-induced vasoconstriction in ocular vessels is caused by V1-receptor mediated signaling pathways. The V2-antagonist showed no effect at the selected concentrations. Further studies have to prove if different concentrations of AVP and V2-antagonist influence ocular blood flow, respectively.
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