Alteração de perfil de citocinas inflamatórias na hipertensão

Autores

  • Fernando Alves Santa Rosa fernandoasr78@gmail.com
    UNINOVE

DOI:

10.24281/rremecs.2018.04.11.se34-36

Resumo

O conceito de que o sistema imunológico contribui para a hipertensão não é novo. Em estudo pioneiro os pesquisadores, descreveram o papel da terapia imunossupressora sobre os níveis de PA em ratos com infarto renal1. Ouros estudiosos, mostraram que as células T são essenciais para o pleno desenvolvimento de hipertensão arterial sistêmica (HAS) dependente de Angiotensina II (AngII) em ratos scid imunodeficientes2.

Biografia do Autor

Fernando Alves Santa Rosa, UNINOVE

Docente do Curso de Educação Física da Faculdade Estácio de Carapicuíba. Laboratório de Fisiologia Translacional, UNINOVE, São Paulo, SP.

Referências

White FN, Grollman A. Autoimmune factors associated with infarction of the kidney. Nephron. 1964; 1:93-102.

Crowley SD, et al. Lymphocyte responses exacerbate angiotensin II-dependent hypertension. Am J Physiol Regul

Integr Comp Physiol. 2010; 298(4):R1089-97.

Moore JP, et al. M2 macrophage accumulation in the aortic wall during angiotensin II infusion in mice is associated with fibrosis, elastin loss, and elevated blood pressure. Am J Physiol Regul Integr Comp Physiol. 2015;

(5):H906-17.

Wenzel P, et al. Lysozyme M–positive monocytes mediate angiotensin II–induced arterial hypertension and vascular dysfunction. Circulation. 2011; 124(12):1370-81.

Weber C, et al. Role and analysis of monocyte subsets in cardiovascular disease. Thromb Haemost. 2016;

(4):626-37.

Nosalski R, Guzik TJ. Perivascular adipose tissue inflammation in vascular disease. Br J Pharmacol. 2017;

(20):3496-3513.

Levy D, et al. Genome-wide association study of blood pressure and hypertension. Nat Genet. 2009; 41(6):677-

Saleh MA, et al. Lymphocyte adaptor protein LNK deficiency exacerbates hypertension and end-organ inflammation. J Clin Invest. 2015; 125(3):1189-202.

Boos CJ, Lip GY. Is hypertension an inflammatory process? Curr Pharm Des. 2006; 12(13):1623-35.

Bautista LE. Inflammation, endothelial dysfunction, and the risk of high blood pressure: epidemiologic and biological evidence. J Hum Hypertens. 2003; 17(4):223-30.

Saito M, et al. Relations of plasma high-sensitivity C-reactive protein to traditional cardiovascular risk factors. Atherosclerosis. 2003; 167(1):73-9.

Torzewski J, et al. C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. Arterioscler Thromb Vasc Biol. 1998; 18(9):1386-

Bautista LE, et al. Independent association between inflammatory markers (C-reactive protein, interleukin-6, and TNF-α) and essential hypertension. J Hum Hypertens. 2005; 19(2):149-54.

London GM. Role of arterial wall properties in the pathogenesis of systolic hypertension. American Journal of

Hypertension. 2005; 18(1):19S-22S.

Verma S, Anderson TJ. Fundamentals of endothelial function for the clinical cardiologist. Circulation. 2002;

(5):546-9.

Nadar S, Lip GY. The prothrombotic state in hypertension and the effects of antihypertensive treatment. Curr

Pharm Des. 2003; 9(21):1715-32.

Pedrinelli R. Endothelial vasomotor dysfunction in hypertension. J Hum Hypertens. 2000; 14(8):481-3.

Klahr S. The role of nitric oxide in hypertension and renal disease progression. Nephrol Dial Transplant. 2001;

Suppl 1:60-2.

Brunini TM, et al. Diminished L-arginine bioavailability in hypertension. Clin Sci (Lond). 2004; 107(4):391-7.

Publicado

31-05-2018
Métricas
  • Visualizações 0
  • PDF downloads: 0

Como Citar

ALVES SANTA ROSA, F. . Alteração de perfil de citocinas inflamatórias na hipertensão. Revista Remecs - Revista Multidisciplinar de Estudos Cientí­ficos em Saúde, [S. l.], p. 34–36, 2018. DOI: 10.24281/rremecs.2018.04.11.se34-36. Disponível em: http://revistaremecs.com.br/index.php/remecs/article/view/108. Acesso em: 13 set. 2024.

Edição

Seção

Resumos Expandidos