Abstract:
: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.
journal_name
Int J Hypertensjournal_title
International journal of hypertensionauthors
Dugaich AP,Oliveira-Sales EB,Abreu NP,Boim MA,Bergamaschi CT,Campos RRdoi
10.4061/2010/219358subject
Has Abstractpub_date
2011-01-04 00:00:00pages
219358eissn
2090-0384issn
2090-0392journal_volume
2010pub_type
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journal_title:International journal of hypertension
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journal_title:International journal of hypertension
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