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The role of central ROS and NO in aldosterone (ALDO)/salt‐induced hypertension
Author(s) -
Xue Baojian,
BadauePassos Daniel,
Beltz Terry G.,
Bhalla Ramesh C.,
Hay Meredith,
Johnson Alan Kim
Publication year - 2009
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.23.1_supplement.956.4
Subject(s) - apocynin , medicine , mineralocorticoid , endocrinology , aldosterone , reactive oxygen species , nitric oxide , mineralocorticoid receptor , blood pressure , chemistry , nadph oxidase , oxidative stress , biochemistry
It has been shown that increased reactive oxygen species (ROS) production in kidneys and blood vessels contributes to elevated blood pressure (BP) in rats with mineralocorticoid excess. Nitric oxide (NO) also plays an important role in the regulation of ROS production and BP. However, the role of ROS and NO in the brain in the pathophysiology of mineralocorticoid excess is not fully understood. In the present study, we tested the hypothesis that central ROS and NO production is involved in the BP increase produced by ALDO/salt treatment. BP was measured in male and female rats with the use of telemetry implants. Rats were infused with ALDO (0.75 μg/h, 28 days) via an osmotic pump implanted subcutaneously and given access to 1% NaCl as the sole drinking fluid. ICV, but not subcutaneous, infusions of apocynin (4 μg/kg/min) for 28 days attenuated ALDO/salt‐induced hypertension in male rats (central n=3, Δ16.5± 2.3 vs peripheral n=2, Δ30.4 ± 4.1 mmHg). In a parallel study, ICV L‐NAME infusion (50 μg/kg/day) enhanced the pressor effects in ALDO/salt‐treated female rats (n=3, Δ21.7±1.1 mmHg) when compared to ALDO/salt‐treated females with peripheral L‐NAME (n=2, Δ10.6±1.2 mmHg). Central infusions of apocynin alone or of L‐NAME alone had no effect on BP. These results suggest that increased ROS and/or decreased NO in the central nervous system play an important role in the development of ALDO/salt‐induced hypertension. (Support: NIH HL‐59676, HL‐62261, HL‐14388, & DK‐66086)