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OXIDATIVE STRESS IN SYMPATHETIC PREMOTOR NEURONS CONTRIBUTES TO RENOVASCULAR HYPERTENSION
Author(s) -
OliveiraSales Elizabeth Barbosa,
Nishi Erika Emy,
Boim Mirian Aparecida,
Dolnikoff Miriam Sterman,
Bergamaschi Cássia Toledo,
Campos Ruy Ribeiro
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.968.9
Subject(s) - rostral ventrolateral medulla , oxidative stress , medicine , endocrinology , vasomotor , reactive oxygen species , superoxide , superoxide dismutase , chemistry , nadph oxidase , blood pressure , heart rate , enzyme , biochemistry
Based on previous data, we hypothesized that overactivity of NAD(P)H oxidase‐derived reactive oxygen species and lowered activity of CuZnSOD, an endogenous antioxidant within the rostral ventrolateral medulla (RVLM), could contribute to 2K‐1C hypertension. Using real‐time PCR, we found that mRNA expression of NAD(P)H oxidase subunits (p47phox and gp91phox) was greater in 2K‐1C compared to the control group in the RVLM and CuZnSOD expression was similar in both groups. To test the functional significance of whether oxidative stress was involved in the maintenance of sympathetic vasomotor tone and blood pressure in 2K‐1C, we injected (1 and 5 nmol/100nl) of superoxide dismutase mimetic (Tempol) into the RVLM. In 2K‐1C, Tempol ‐1nmol resulted in a higher fall in mean arterial pressure (MAP) than the other dose (15 ± 1%, P <0,05) followed by a significant reduction in renal sympathetic nerve activity (RSNA) (11± 2%). Tempol 5 nmol decreased MAP 12± 4% ( P <0,05) and RSNA 20 ±7% ( P <0,05). In the control group, all doses of Tempol did not change MAP, however, Tempol 1 and 5 nmol decreased RSNA (6 ± 2%, 2 ± 2%, respectively). Taken altogether, the results support the idea that an increase in oxidative stress within the RVLM plays a major role in maintaining hypertension and sympathetic drive in 2K‐1C. Supported by FAPESP.