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Pernille Oversoe Hansen, Sidse Kringelholt, Ulf Simonsen, Toke Bek; Hypoxia induced relaxation of porcine retinal arterioles in vitro depends on nitric oxide and stimulation of EP4-receptors in the perivascular retina. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4345.
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© ARVO (1962-2015); The Authors (2016-present)
Previous studies have shown that the inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX) can reduce hypoxia induced relaxation of retinal arterioles in vitro. However, the identity of the NOS and COX products involved in the response are unknown.
Porcine retinal arterioles with preserved perivascular retinal tissue mounted in a myograph were exposed to hypoxia in the presence of one of the following: The general NO synthase inhibitor L-NAME, the selective iNOS inhibitor 1400W, the selective nNOS inhibitor 7-Nitroindazole, the general COX inhibitor Ibuprofen, or antagonist to the FP- (AL 8810), DP- (BW868A), EP1- (SC-19220), EP2- (PF-044189) or EP4-receptors (GW627368X). The experiments were repeated after removal of the perivascular retinal tissue.
Hypoxia induced significant relaxation of retinal arterioles in the presence of perivascular retinal tissue. This relaxation was significantly reduced in the presence of L-NAME, 1400W, Ibuprofen and the EP4-receptor antagonist GW627368X.
Hypoxia induced relaxation of retinal arterioles depends on nitric oxide produced by iNOS and an effect of COX products mediated by EP4-receptors in the perivascular retinal tissue.
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