Reactive oxygen species derived from NAD(P) H oxidase play a role on ethanol-induced hypertension and endothelial dysfunction in rat resistance arteries

被引:26
作者
Simplicio, Janaina A. [1 ,2 ]
do Vale, Gabriel T. [1 ,2 ]
Gonzaga, Natalia A. [1 ,2 ]
Leite, Leticia N. [1 ,2 ]
Hipolito, Ulisses V. [2 ]
Pereira, Camila A. [1 ]
Tostes, Rita C. [1 ]
Tirapelli, Carlos R. [2 ]
机构
[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, Ribeirao Preto, SP, Brazil
[2] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, DEPCH, Lab Farmacol, Ave Bandeirantes 3900, BR-14040902 Ribeirao Preto, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
Ethanol; Oxidative stress; Superoxide anion; Hypertension; Apocynin; VASCULAR OXIDATIVE STRESS; ACTIVATED PROTEIN-KINASE; BLOOD-PRESSURE; ANGIOTENSIN-II; TRANSGENIC MICE; CONSUMPTION; LIVER; INTERLEUKIN-10; EXPRESSION; RECEPTOR;
D O I
10.1007/s13105-016-0519-z
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chronic ethanol consumption is a risk factor for cardiovascular diseases. We studied whether NAD(P) H oxidasederived reactive oxygen species (ROS) play a role in ethanol-induced hypertension, vascular dysfunction, and protein expression in resistance arteries. Male Wistar rats were treated with ethanol (20 % v/v) for 6 weeks. Ethanol treatment increased blood pressure and decreased acetylcholine-induced relaxation in the rat mesenteric arterial bed (MAB). These responses were attenuated by apocynin (30 mg/kg/day; p. o. gavage). Ethanol consumption increased superoxide anion (O-2(-)) generation and decreased nitrate/nitrite (NOx) concentration in the rat MAB and apocynin prevented these responses. Conversely, ethanol did not affect the concentration of hydrogen peroxide (H2O2) and reduced glutathione (GSH) or the activity of superoxide dismutase (SOD) and catalase (CAT) in the rat MAB. Ethanol increased interleukin (IL)-10 levels in the rat MAB but did not affect the levels of tumor necrosis factor (TNF)-alpha, IL-6, or IL1 beta. Ethanol increased the expression of Nox2 and the phosphorylation of SAPK/JNK, but reduced eNOS expression in the rat MAB. Apocynin prevented these responses. However, ethanol treatment did not affect the expression of Nox1, Nox4, p38MAPK, ERK1/2, or SAPK/JNK in the rat MAB. Ethanol increased plasma levels of TBARS, TNF-alpha, IL-6, IL-1 beta, and IL-10, whereas it decreased NOx levels. The major finding of our study is that NAD(P) H oxidase-derived ROS play a role on ethanol-induced hypertension and endothelial dysfunction in resistance arteries. Moreover, ethanol consumption affects the expression and phosphorylation of proteins that regulate vascular function and NAD(P)H oxidase-derived ROS play a role in such responses.
引用
收藏
页码:5 / 16
页数:12
相关论文
共 45 条
[1]   Endothelial Nox2 overexpression potentiates vascular oxidative stress and hemodynamic response to angiotensin II - Studies in endothelial-targeted Nox2 transgenic mice [J].
Bendall, Jennifer K. ;
Rinze, Ruth ;
Adlam, David ;
Tatham, Amy L. ;
de Bono, Joe ;
Channon, Keith M. .
CIRCULATION RESEARCH, 2007, 100 (07) :1016-1025
[2]   INCREASED PLASMA TUMOR-NECROSIS-FACTOR IN SEVERE ALCOHOLIC HEPATITIS [J].
BIRD, GLA ;
SHERON, N ;
GOKA, AKJ ;
ALEXANDER, GJ ;
WILLIAMS, RS .
ANNALS OF INTERNAL MEDICINE, 1990, 112 (12) :917-920
[3]   Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress [J].
Carda, Ana P. P. ;
Marchi, Katia C. ;
Rizzi, Elen ;
Mecawi, Andre S. ;
Antunes-Rodrigues, Jose ;
Padovan, Claudia M. ;
Tirapelli, Carlos R. .
STRESS-THE INTERNATIONAL JOURNAL ON THE BIOLOGY OF STRESS, 2015, 18 (02) :233-243
[4]   Intracellular antioxidants:: from chemical to biochemical mechanisms [J].
Chaudière, J ;
Ferrari-Iliou, R .
FOOD AND CHEMICAL TOXICOLOGY, 1999, 37 (9-10) :949-962
[5]   Nox1 overexpression potentiates angiotensin II-induced hypertension and vascular smooth muscle hypertrophy in transgenic mice [J].
Dikalova, A ;
Clempus, R ;
Lassègue, B ;
Cheng, GJ ;
McCoy, J ;
Dikalov, S ;
Martin, AS ;
Lyle, A ;
Weber, DS ;
Weiss, D ;
Taylor, R ;
Schmidt, HHHW ;
Owens, GK ;
Lambeth, JD ;
Griendling, KK .
CIRCULATION, 2005, 112 (17) :2668-2676
[6]   INFLUENCE OF NG-MONOMETHYL-L-ARGININE ON ENDOTHELIUM-DEPENDENT RELAXATIONS IN THE PERFUSED MESENTERIC VASCULAR BED OF THE RAT [J].
EBEIGBE, AB ;
CRESSIER, F ;
KONNEH, MK ;
LUU, TD ;
CRISCIONE, L .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 169 (03) :873-879
[7]   Long-term alcohol exposure changes sensitivity of rat Kupffer cells to lipopolysaccharide [J].
Enomoto, N ;
Schemmer, P ;
Ikejima, K ;
Takei, Y ;
Sato, N ;
Brenner, DA ;
Thurman, RG .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 2001, 25 (09) :1360-1367
[8]  
FAHIMI HD, 1979, AM J PATHOL, V96, P373
[9]   Ethanol withdrawal increases oxidative stress and reduces nitric oxide bioavailability in the vasculature of rats [J].
Gonzaga, Natalia A. ;
Mecawi, Andre S. ;
Antunes-Rodrigues, Jose ;
De Martinis, Bruno S. ;
Padovan, Claudia M. ;
Tirapelli, Carlos R. .
ALCOHOL, 2015, 49 (01) :47-56
[10]   Acute ethanol intake induces mitogen-activated protein kinase activation, platelet-derived growth factor receptor phosphorylation, and oxidative stress in resistance arteries [J].
Gonzaga, Natalia A. ;
Callera, Glaucia E. ;
Yogi, Alvaro ;
Mecawi, Andre S. ;
Antunes-Rodrigues, Jose ;
Queiroz, Regina H. ;
Touyz, Rhian M. ;
Tirapelli, Carlos R. .
JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY, 2014, 70 (02) :509-523