BACKGROUND AND PURPOSE: Our goal was to determine whether NAD(P)H oxidase is involved in impaired endothelial nitric oxide synthase (eNOS)-dependent reactivity of cerebral arterioles during chronic alcohol consumption. METHODS: Sprague-Dawley rats were fed with an alcohol diet for 2 to 3 months. We determined the effects of acute and chronic treatment with an NAD(P)H oxidase inhibitor, apocynin, on responses of pial arterioles to eNOS-dependent agonists (acetylcholine and ADP) and an eNOS-independent agonist (nitroglycerin). Expression of NAD(P)H oxidase in pial arterioles was measured with the use of real-time polymerase chain reaction and Western blot analysis, and superoxide production was measured with the use of lucigenin-enhanced chemiluminescence. RESULTS: Vasodilation in response to acetylcholine and ADP, but not nitroglycerin, was significantly less in alcohol-fed rats. Treatment with apocynin did not alter vasodilation in non-alcohol-fed rats but significantly improved impaired vasodilation in alcohol-fed rats. In addition, an upregulation of p47phox in pial arterioles was found in alcohol-fed rats. Furthermore, alcohol consumption increased superoxide production under basal conditions and in the presence of ADP and NAD(P)H. CONCLUSIONS: Our findings suggest that NAD(P)H oxidase plays a role in chronic alcohol consumption-induced impairment of eNOS-dependent dilation of cerebral arterioles.
BACKGROUND AND PURPOSE: Our goal was to determine whether NAD(P)H oxidase is involved in impaired endothelial nitric oxide synthase (eNOS)-dependent reactivity of cerebral arterioles during chronic alcohol consumption. METHODS:Sprague-Dawley rats were fed with an alcohol diet for 2 to 3 months. We determined the effects of acute and chronic treatment with an NAD(P)H oxidase inhibitor, apocynin, on responses of pial arterioles to eNOS-dependent agonists (acetylcholine and ADP) and an eNOS-independent agonist (nitroglycerin). Expression of NAD(P)H oxidase in pial arterioles was measured with the use of real-time polymerase chain reaction and Western blot analysis, and superoxide production was measured with the use of lucigenin-enhanced chemiluminescence. RESULTS: Vasodilation in response to acetylcholine and ADP, but not nitroglycerin, was significantly less in alcohol-fed rats. Treatment with apocynin did not alter vasodilation in non-alcohol-fed rats but significantly improved impaired vasodilation in alcohol-fed rats. In addition, an upregulation of p47phox in pial arterioles was found in alcohol-fed rats. Furthermore, alcohol consumption increased superoxide production under basal conditions and in the presence of ADP and NAD(P)H. CONCLUSIONS: Our findings suggest that NAD(P)H oxidase plays a role in chronic alcohol consumption-induced impairment of eNOS-dependent dilation of cerebral arterioles.
Authors: Saleena Alikunju; P M Abdul Muneer; Yan Zhang; Adam M Szlachetka; James Haorah Journal: Brain Behav Immun Date: 2011-01-22 Impact factor: 7.217
Authors: Cynthia M Lynch; Dale A Kinzenbaw; Xunxheng Chen; Shanshan Zhan; Erin Mezzetti; Jessica Filosa; Adviye Ergul; Jessica L Faulkner; Frank M Faraci; Sean P Didion Journal: Stroke Date: 2013-09-26 Impact factor: 7.914
Authors: Dean J Kleinhenz; Roy L Sutliff; John A Polikandriotis; Erik R Walp; Sergey I Dikalov; David M Guidot; C Michael Hart Journal: Alcohol Clin Exp Res Date: 2007-11-20 Impact factor: 3.455