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Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Michigan 48202-2689
Although NAD(P)H oxidase-derived superoxide
(O2
) is increased during the development of
angiotensin II (ANG II)-dependent hypertension, vascular regulation at
the protein level has not been reported. We have shown that four major
components of NAD(P)H oxidase are located primarily in the vascular
adventitia as a primary source of vascular O2. Here
we compare vascular levels of O2 and NAD(P)H oxidase
in normotensive and ANG II-infused hypertensive mice and show that,
after 7 days of ANG II infusion (750 µg · kg1 · day1 ip) in
C57B1/6 mice, systolic blood pressure was increased compared with that
after sham infusion, concomitant with increased O2 in
the thoracic aorta as measured using lucigenin (25 µM)-enhanced chemiluminescence. Both p67phox and
gp91phox were detectable by Western blotting in
aortic homogenates, and we observed increased protein levels of
NAD(P)H oxidase subunits. These ANG II-induced increases were
normalized by simultaneous treatment with the AT1
receptor antagonist losartan. Moreover, the primary location of these
subunits was the adventitia as detected immunohistochemically. Our
results suggest that ANG II-induced increases in O2
are due to increased adventitial NAD(P)H oxidase activity, brought about by the heightened expression and interaction of its components.
hypertension; superoxide anion; free radicals; reactive oxygen species; NAD(P)H oxidase; NAD(P)H oxidoreductase
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