ET-1-induced oxidative stress in doca-salt hypertension involves NAD(P)H oxidase-independent mechanisms (2005)
- Authors:
- Autor USP: PASSAGLIA, RITA DE CASSIA ALEIXO TOSTES - ICB
- Unidade: ICB
- Assunto: FARMACOLOGIA
- Language: Português
- Abstract: Objetivo: Vascular oxidative stress in DOCA rats is associated with activation of the endothelin system via ETA receptors. The exact source of endothelin-1 (ET-1)-mediated oxidative stress remains unclear. We investigated whether ET-1 increases generation of reactive oxygen species (ROS) in DOCA hypertension through NAD(P)H oxidase-dependent mechanisms. Xanthine oxidase and nitric oxide synthase (eNOS) were also questioned as potential ET-1 sources of vascular ROS. Métodos e Resultados: DOCA and control (UniNX) rats were treated with the ETA antagonist BMS 182874 (40 mg/kg per day) or vehicle. Systemic oxidative stress, evaluated by plasma thiobarbituric acid-reacting substances (TBARS), was increased in DOCA (1.6±0.1 umol/mL) vs. UniNX (1.1±0.05 umol/mL, p<0.05) rats. Activity of NAD(P)H and xanthine oxidases (arbitrary units/mg protein) in mesenteric arteries [NAD(P)H, UniNx: 1564±223 vs. DOCA: 2660±395; Xanthine, UniNx: 590±133 vs.DOCA: 1070±77], aorta and heart was increased (p<0.05) in DOCA rats. BMS decreased plasma TBARs levels without influencing NAD(P)H and xanthine oxidase activities in DOCA rats. Assessment of gene and protein expression of NAD(P)H subunits, showed an increase in p22phox (D: 90±13 vs. C: 56±8 arbitrary units) without changes in p47phox in arteries from DOCA rats. Increased p47phox membrane (Cytosol, C: 128±14; D: 76±12; vs. Membrane, C: 22±6, D: 61±16 arbitrary units) translocation was observed in DOCA aortas. BMS did not affect theincrease in p22phox expression nor p47phox translocation. Increased eNOS expression in DOCA aortas (96±9 vs. C: 31±9 arbitrary units) was unaltered by BMS. Conclusões: Activation of NAD(P)H oxidase does not seem to be a major source of oxidative stress induced by ET-1/ETA in DOCA-salt hypertension and appears to be also independent of increased activation of xanthine oxidase or eNOS overexpression.
- Imprenta:
- Publisher: Federação de Sociedades de Biologia Experimental
- Publisher place: Águas de Lindóia, São Paulo
- Date published: 2005
- Source:
- Título do periódico: Resumos
- Conference titles: Reunião Anual da Federação de Sociedades de Biologia Experimental, FeSBE
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ABNT
CALLERA, G. E. et al. ET-1-induced oxidative stress in doca-salt hypertension involves NAD(P)H oxidase-independent mechanisms. 2005, Anais.. Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental, 2005. . Acesso em: 19 set. 2024. -
APA
Callera, G. E., Passaglia, R. de C. A. T., Yogi, A., Montezano, A. C., & Touyz, R. M. (2005). ET-1-induced oxidative stress in doca-salt hypertension involves NAD(P)H oxidase-independent mechanisms. In Resumos. Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental. -
NLM
Callera GE, Passaglia R de CAT, Yogi A, Montezano AC, Touyz RM. ET-1-induced oxidative stress in doca-salt hypertension involves NAD(P)H oxidase-independent mechanisms. Resumos. 2005 ;[citado 2024 set. 19 ] -
Vancouver
Callera GE, Passaglia R de CAT, Yogi A, Montezano AC, Touyz RM. ET-1-induced oxidative stress in doca-salt hypertension involves NAD(P)H oxidase-independent mechanisms. Resumos. 2005 ;[citado 2024 set. 19 ] - Novos mecanismos moleculares da hipertensão, sistema endotelia na hipertensão arterial
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