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Renal denervation reduces sympathetic overactivation, brain oxidative stress, and renal injury in rats with renovascular hypertension independent of its effects on reducing blood pressure

Texto completo
Nishi, Erika E. [1] ; Lopes, Nathalia R. [1] ; Gomes, Guiomar N. [1] ; Perry, Juliana C. [2] ; Sato, Alex Y. S. [1] ; Naffah-Mazzacoratti, Maria G. [3] ; Bergamaschi, Cassia T. [1] ; Campos, Ruy R. [1]
Número total de Autores: 8
Afiliação do(s) autor(es):
[1] Univ Fed Sao Paulo, Dept Physiol, Escola Paulista Med, Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Dept Psychobiol, Escola Paulista Med, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Neurol & Neurosurg, Escola Paulista Med, Sao Paulo - Brazil
Número total de Afiliações: 3
Tipo de documento: Artigo Científico
Fonte: HYPERTENSION RESEARCH; v. 42, n. 5, p. 628-640, MAY 2019.
Citações Web of Science: 5

The underlying mechanisms by which renal denervation (RD) decreases blood pressure (BP) remain incompletely understood. In this study, we investigated the effects of ischemic kidney denervation on different sympathetic outflows, brain and renal expression of angiotensin-II receptors, oxidative stress and renal function markers in the 2-kidney, 1-clip (2K-1C) rat model. Surgical RD was performed in Wistar male rats 4-5 weeks after clip implantation. After 10 days of RD, BP, and the activity of sympathetic nerves projecting to the contralateral kidney (rSNA) and splanchnic region were partially reduced in 2K-1C rats, with no change in systemic renin-angiotensin system (RAS). To distinguish the effects of RD from the reduction in BP, 2K-1C rats were treated with hydralazine by oral gavage (25 mg/kg/day for 1 week). RD, but not hydralazine, normalized oxidative stress in the sympathetic premotor brain regions and improved intrarenal RAS, renal injury, and proteinuria. Furthermore, different mechanisms led to renal injury and oxidative stress in the ischemic and contralateral kidneys of 2K-1C rats. Injury and oxidative stress in the ischemic kidney were driven by the renal nerves. Although RD attenuated rSNA, injury and oxidative stress persisted in the contralateral kidney, probably due to increased BP. Therefore, nerves from the ischemic kidney at least partially contribute to the increase in BP, sympathetic outflows, brain oxidative stress, and renal alterations in rats with renovascular hypertension. Based on these findings, the reduction in oxidative stress in the brain is a central mechanism that contributes to the effects of RD on Goldblatt hypertension. (AU)

Processo FAPESP: 13/22522-9 - Papel do nervo simpático renal nas alterações cardiovasculares e renais na hipertensão arterial renovascular
Beneficiário:Ruy Ribeiro de Campos Junior
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 10/09003-4 - Papel da atividade nervosa simpática renal na hipertensão renovascular experimental
Beneficiário:Erika Emy Nishi
Linha de fomento: Bolsas no Brasil - Doutorado
Processo FAPESP: 15/23858-6 - Efeitos da denervação renal sobre o estresse oxidativo renal na hipertensão renovascular experimental
Beneficiário:Nathalia Rodrigues Lopes
Linha de fomento: Bolsas no Brasil - Iniciação Científica