Role of the Rostral Ventrolateral Medulla in the Arterial Hypertension in Chronic Renal Failure

Adriana P. Castilho Dugaich, Elizabeth B. Oliveira-Sales, Nayda P. Abreu, Mirian A. Boim, C´assia T. Bergamaschi, and Ruy R. Campos SAGE-Hindawi Access to Research International Journal of Hypertension Volume 2010, Article ID 219358, 6 pages doi:10.4061/2010/219358 It has been purposed that during chronic renal failure (CRF) there is an increase in reactive oxygen species (ROS). This may occur because ang II leads to an increased activity of NAD(P)H oxidase, which is responsible for the majority of superoxide that are produced. NAD(P)H is composed of gp91phox and p22 phox. The cytoplasmic components are p40phox p47phox, p67phox and the small G protein Racla. When ang II binds to AT1 receptor this leads to the cytoplasmic units binding to the membrane subunits and activating the NAD(P)H enzyme and this leads to the production of O2-. The purpose of this study is to quantify p47phox and gp91phox expression in RVLM, along with AT1 receptor expression in the RVLM. They also want to identify the role of AT1 in the superoxide production. So they injected candestan an AT1 antagonist. They also scavenged for superoxides by injecting tempol. Finally they tested inhibitory signaling specifically they looked at GABAergic responsiveness in the RVLM, by giving GABA./they found that AT1 mRNA was significantly decreased in CRF compared to controls in the brainstem. P47phox and gp91phox gene expression in RVLM in CRF group was significantly higher compared to controls. As for the microinjection portion of the study they found that Tempol resulted in decreases in MAP in CRF and not in controls. Also GABA caused larger decreases in MAP in CRF compared to controls. The candestan did not significantly change MAP. These data suggest that there is an increase in superoxide production but it is not due to AT1 receptor activation.-MD