Open AccessExpression of NAD(P)H Oxidase Subunits and Their Contribution to Cardiovascular Damage in Aldosterone/Salt-Induced Hypertensive Rat
Author(s) -
Young Mee Park,
Bong Hee Lim,
Rhian M. Touyz,
Jeong Bae Park
Publication year - 2008
Publication title -
journal of korean medical science/journal of korean medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.743
H-Index - 66
eISSN - 1598-6357
pISSN - 1011-8934
DOI - 10.3346/jkms.2008.23.6.1039
Subject(s) - aldosterone , apocynin , losartan , spironolactone , mineralocorticoid receptor , endocrinology , medicine , mineralocorticoid , nad(p)h oxidase , chemistry , aldosterone synthase , nad+ kinase , oxidase test , nadph oxidase , renin–angiotensin system , angiotensin ii , receptor , biochemistry , enzyme , oxidative stress , blood pressure
NAD(P)H oxidase plays an important role in hypertension and its complication in aldosterone-salt rat. We questioned whether NAD(P)H oxidase subunit expression and activity are modulated by aldosterone and whether this is associated with target-organ damage. Rats were infused with aldosterone (0.75 microg/hr/day) for 6 weeks and were given 0.9% NaCl+/-losartan (30 mg/kg/day), spironolactone (200 mg/kg/day), and apocynin (1.5 mM/L). Aldosterone-salt hypertension was prevented completely by spironolactone and modestly by losartan and apocynin. Aldosterone increased aortic NAD(P)H oxidase activity by 34% and spironolactone and losartan inhibited the activity. Aortic expression of the subunits p47(phox), gp91(phox), and p22(phox) increased in aldosterone-infused rats by 5.5, 4.7, and 3.2-fold, respectively, which was decreased completely by spironolactone and partially by losartan and apocynin. Therefore, the increased expression of NAD(P)H oxidase may contribute to cardiovascular damage in aldosterone-salt hypertension through the increased expression of each subunit.