Qin Fang

University of Nebraska at Omaha, Omaha, NE, United States

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Publications (6)24.7 Total impact

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    ABSTRACT: Our goals were to determine whether chronic exposure to nicotine alters nitric oxide synthase (NOS)-dependent reactivity of cerebral (pial) arterioles and to identify a potential role for NADPH oxidase in impaired NOS-dependent responses during chronic exposure to nicotine. We measured in vivo diameter of pial arterioles to NOS-dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists in saline-treated rats and rats chronically treated with nicotine (2 mg.kg(-1).day(-1) for 2 wk via an osmotic minipump). We found that NOS-dependent, but not -independent, vasodilatation was impaired in nicotine-treated compared with saline-treated rats. In addition, the production of superoxide anion (lucigenin chemiluminescence) was increased in rats treated with nicotine compared with saline-treated rats. Furthermore, using Western blot analysis, we found that chronic exposure to nicotine increased p47phox protein in the parietal cortex. Finally, we found that apocynin (40 mg.kg(-1).day(-1)) in the drinking water to inhibit NADPH oxidase alleviated impaired NOS-dependent cerebral vasodilatation in nicotine treated rats but did not alter NOS-dependent responses in saline treated rats and did not alter NOS-independent reactivity in saline- or nicotine-treated rats. These findings suggest that chronic exposure to nicotine impairs NOS-dependent dilatation of pial arterioles by a mechanism that appears to be related to the formation of superoxide anion via activation of NADPH oxidase.
    Journal of Applied Physiology 03/2006; 100(2):631-6. · 3.43 Impact Factor
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    ABSTRACT: 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. 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. 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. Our findings suggest that NAD(P)H oxidase plays a role in chronic alcohol consumption-induced impairment of eNOS-dependent dilation of cerebral arterioles.
    Stroke 03/2006; 37(2):495-500. · 6.02 Impact Factor
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    ABSTRACT: The goal of the present study was to determine the role of NAD(P)H oxidase in alcohol consumption-induced impairment of nNOS-dependent reactivity in cerebral arterioles. Sprague-Dawley rats were fed an alcohol diet for 2-3 months. We measured the effects of acute (1 hour) and chronic (1 month) treatment with a NAD(P)H oxidase inhibitor, apocynin, on responses of parietal pial arterioles to nNOS-dependent agonists (NMDA and kainate) and an nitric oxide synthase (NOS)-independent agonist (nitroglycerin). In addition, we measured the expression of NAD(P)H oxidase subunits and superoxide production in parietal cortex. Topical application of NMDA and kainate produced dose-related dilation of pial arterioles. However, the magnitude of vasodilation to these agonists was significantly less in alcohol-fed rats. Treatment with apocynin (acute and chronic) did not alter vasodilation in nonalcohol-fed rats, but significantly improved vasodilation in alcohol-fed rats. Response of pial arterioles to nitroglycerin was similar in nonalcohol-fed and alcohol-fed rats, and was not affected by apocynin. In addition, we found an up-regulation of gp91phox and p47phox in parietal cortex of alcohol-fed rats. Finally, alcohol consumption produced an increase in superoxide production under basal conditions and in the presence of NADPH. Acute treatment with apocynin suppressed alcohol consumption-induced superoxide generation. Our findings suggest that NAD(P)H oxidase plays an important role in chronic alcohol consumption-induced impairment of nNOS-dependent dilation of cerebral arterioles.
    Journal of Molecular and Cellular Cardiology 03/2006; 40(2):321-8. · 5.22 Impact Factor
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    ABSTRACT: Exogenous treatment with L-arginine has been shown to restore impaired nitric oxide synthase (NOS)-dependent dilatation of peripheral blood vessels during disease states. We have shown that nicotine impairs NOS-dependent arteriolar dilatation in the cerebral circulation. However, the role of L-arginine in impaired responses of cerebral arterioles during infusion of nicotine has not been examined. Thus the goal of the present study was to examine the role of L-arginine in nicotine-induced impairment of cerebral arteriolar reactivity. We measured the diameter of pial arterioles in response to NOS-dependent (5'-adenosine diphosphate [ADP] and acetylcholine) and NOS-independent (nitroglycerin) agonists before and after infusion of vehicle or nicotine (2 microg/kg/min intravenously for 30 min followed by a maintenance dose of 0.35 microg/kg/min) in the absence or presence of L-arginine (10(-3) M). We found that topical application of L-arginine to cerebral microvessels during infusion of nicotine could prevent impaired NOS-dependent vasodilatation. We suggest that exogenous L-arginine may have a beneficial role in preventing cerebral microvascular dysfunction during exposure to nicotine.
    Nicotine & Tobacco Research 01/2005; 6(6):1009-14. · 2.81 Impact Factor
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    ABSTRACT: The goals of this study were to determine whether chronic alcohol consumption alters potassium channel-mediated reactivity in the basilar artery and to determine a potential mechanism that might account for the effects of alcohol on the basilar artery. Sprague-Dawley rats were fed liquid diets with or without alcohol for 2 to 3 months. We measured diameter of the basilar artery in response to potassium channel inhibitors and activators. Protein level of inward rectifier potassium channel subunit Kir2.1 in the basilar artery was determined by Western blot. Topical application of glibenclamide (1 and 10 microM) significantly constricted the basilar artery at high dose; iberiotoxin (10 and 100 nM), 4-AP (0.1 and 1 mM), and BaCl2 (1 and 10 microM) produced dose-related constriction in both non-alcohol-fed and alcohol-fed rats. However, the magnitude of constriction in response to BaCl2 was significantly less in alcohol-fed rats compared with non-alcohol-fed rats. Topical application of KCl (1 and 3 mM), cromakalim (0.1 and 0.3 microM), and NS1619 (10 and 30 microM) induced dose-related dilation in non-alcohol-fed and alcohol-fed rats. However, the magnitude of vasodilation in response to KCl was significantly less in alcohol-fed rats compared with non-alcohol-fed rats. In addition, Kir2.1 protein level in the basilar artery was significantly reduced in alcohol-fed compared with non-alcohol-fed rats. These findings suggest that chronic alcohol consumption reduces expression of inward rectifier potassium channels and inhibits KIR channel-mediated dilation in the basilar artery.
    Alcoholism Clinical and Experimental Research 11/2004; 28(10):1557-61. · 3.31 Impact Factor
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    ABSTRACT: The effects of nicotine on nitric oxide synthase (NOS)-dependent reactivity of cerebral arterioles remain uncertain. Our first goal was to examine whether infusion of nicotine alters NOS-dependent reactivity of cerebral arterioles. Our second goal was to examine the mechanisms that may account for the effects of nicotine on cerebral arterioles. We measured the diameter of pial arterioles to NOS-dependent (ADP and acetylcholine) and NOS-independent (nitroglycerin) agonists before and after the infusion of nicotine (2 microg x kg(-1) x min(-1) iv for 30 min, followed by a maintenance dose of 0.35 microg x kg(-1) x min(-1)). ADP- and acetylcholine-induced vasodilatation was impaired after the infusion of nicotine. In contrast, nicotine did not alter vasodilatation to nitroglycerin. Next, we examined whether the impaired responses of pial arterioles during infusion of nicotine may be related to oxygen radicals. We found that application of superoxide dismutase or tetrahydrobiopterin during infusion of nicotine could prevent impaired NOS-dependent vasodilatation. Thus acute exposure of cerebral vessels to nicotine specifically impairs NOS-dependent dilatation via the production of oxygen radicals possibly related to an alteration in the utilization of tetrahydrobiopterin.
    AJP Heart and Circulatory Physiology 03/2003; 284(2):H528-34. · 4.01 Impact Factor