Dugaich Adriana P Castilho, Oliveira-Sales Elizabeth B, Abreu Nayda P, Boim Mirian A, Bergamaschi Cássia T, Campos Ruy R
Cardiovascular Division, Department of Physiology, Federal University of São Paulo, São Paulo, SP, Brazil.
Int J Hypertens. 2011 Jan 4;2010:219358. doi: 10.4061/2010/219358.
Sympathetic activation in chronic renal failure (CRF) is a major mechanism leading to the progression of renal disease and hypertension. In the present study, we tested the hypothesis that in CRF increased reactive oxygen species (ROS) production in the RVLM mediated by enhanced circulating Angiotensin II (Ang II) is an important mechanism leading to hypertension in CRF. In CRF rats we found an increase in the abundance of p47(phox) and gp91(phox) mRNA within the RVLM associated with a reduction of Ang II type 1 receptors (AT(1)) mRNA in the brainstem compared to controls (C). Tempol but not candesartan into the RVLM decreased MAP in CRF but not in C rats. GABA into the RVLM decreased MAP in CRF (63 ± 8 mmHg) more intensely than in C (33 ± 3 mmHg). The results suggest that increased oxidative stress within the RVLM has an important participation to maintain hypertension in CRF rats apparently independently of AT(1) Ang II receptors.
慢性肾衰竭（CRF）中的交感神经激活是导致肾脏疾病和高血压进展的主要机制。在本研究中，我们检验了这样一个假设：在CRF中，循环中血管紧张素II（Ang II）增强介导的延髓头端腹外侧区（RVLM）活性氧（ROS）生成增加是导致CRF高血压的重要机制。与对照组（C）相比，在CRF大鼠中，我们发现RVLM内p47（phox）和gp91（phox）mRNA丰度增加，同时脑干中血管紧张素II 1型受体（AT（1））mRNA减少。向RVLM注射Tempol而非坎地沙坦可降低CRF大鼠的平均动脉压（MAP），但对C组大鼠无效。向RVLM注射γ-氨基丁酸（GABA）对CRF大鼠MAP的降低作用（63±8 mmHg）比对C组大鼠（33±3 mmHg）更强。结果表明，RVLM内氧化应激增加在维持CRF大鼠高血压中起重要作用，这显然独立于AT（1）血管紧张素II受体。
