Purchase this article with an account.
S. Weiß, L. Wagenfeld, P. Galambos, G. Richard, M. Klemm, O. Zeitz; Membrane Potential Determines Vascular Effects of Oxidative Stress. Invest. Ophthalmol. Vis. Sci. 2009;50(13):384.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Several ocular diseases including glaucoma and diabetic retinopathy are associated with disturbed regulation of retinal perfusion. Elevated oxygen free radical (OFR) levels have been reported for glaucoma patients and contradictory findings of effects on vascular tone have been reported for OFR. This study intended to investigate if the baseline membrane potential has an effect on OFR mediated vascular response.
The 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). Some vessels were depolarized to -41mV Nernst potential for K+ before radical exposure. The diameter of the vessel was continuously recorded by a digital edge-detection system. For the control experiments a sham radical exposure was done. Diameters before and after radical exposure were compared using a student t-test.
An OH. exposition at physiological rest membrane potential leads to a significant vasodilatation (diameter: 261.8 ± 3.5 µm before OH. vs. 290.4 ± 2.5 µm after OH.; P<0,001; n=14). In contrast, depolarized vessels respond with a vasoconstriction to OFR exposure (199.4 ± 1.7 µm vs. 183.1 ±1.5 µm; P<0.001; n=10). A sole Fe3+ treatment (sham-exposure) did not influence the vessel diameter.
OFR can influence the myogenic tone. Depending on the actual condition of the vessel radicals can induce dilation or constriction. This observation may explain the mentioned contradictory results in literature. Regarding clinical situations, the data show that oxidative stress may lead to a dysregulation of vascular tone in all directions depending of the vessels baseline status. Oxidative stress e.g. in glaucoma or diabetic retinopathy may therefore potentiate its own destructive effect on neuronal tissue by an alteration of ocular perfusion.
This PDF is available to Subscribers Only