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L. Wagenfeld, S. Weiß, M. Klemm, P. Galambos, G. Richard, O. Zeitz; Vascular Effects of Oxidative Stress: Mechanisms of Vasodilation. Invest. Ophthalmol. Vis. Sci. 2009;50(13):391.
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Oxidative stress is involved in the pathogenesis of several ocular diseases like glaucoma. Oxidative stress can induce disturbed ocular blood flow by disrupting myogenic tone. Vasodilative as well as vasoconstricting effects of oxygen free radicals (OFR) can be found in the literature. The vasodilative effects were partially addressed to a hyperpolarizing effect of oxygen radicals, which could be released by the endothelium. This work investigates the involvement of the endothelium and of the Na-K ATPase in the vasodilating effect of OFR.
Our experiments were carried out with rat ophthalmic arteries that were freshly dissected and placed in a perfusion setup. After a reproducible myogenic tone was established at 80 mmHg, the vessel was exposed to oxygen free radicals from the fenton reaction H2O2 and Fe3+ (FeNTA). These experiments were also carried out with endothelium removed vessels. Other vessels were exposed to 10-5 M ouabain a blocker of the Na-K ATPase before OFR were added. The diameter of the vessel was continuously recorded by a digital edge-detection system. The change in diameters provoked by OFR per group was compared using a paired t-test. The Change of diameters provoked by OFR was compared between both groups using an unpaired student t-test.
In accordance to previously published data, our vessels show a stable and reproducible myogenic tone at 80 mmHg. OFR provoke a significant vasodilation in the untreated group (231.0 ± 2.4 µm before OFR vs. 270.5 ± 2.8 µm after OFR; n=11, P<0.001) which can also be found when endothelium was removed (214.9 ± 0.4 µm before OFR vs. 260.1 ± 1.7 µm after OFR; n=5, P=0.01) There can no significant dilation be found in the ouabain treated group (227.0 ± 3.2 µm before OFR vs. 235.8 ± 2.9 µm after OFR; n=13, P=0.1). The change of diameters in percent provoked by OFR exposure was 5.8 ± 2.4 % in the ouabain treated group compared to 15.5 ±1.8 % in the untreated group. This difference was statistically significant, p=0.01, n=11.
OFR can lead to a significant vasodilation under certain conditions. Our findings could support the theory that this vasodilation is determined by a hyperpolarizing effect of OFR and this hyperpolarization could be induced by a stimulation of the Na-K ATPase. In our experiments the endothelium has no influence on the OFR effect.
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