Linz W, Wiemer G, Malinski T, Scholkens BA
Life span extension of genetically hypertensive rats after long
-term ACE-inhibition correlates to enhanced NO-
availability
12th Annual ASH Meeting
Am J Hypertens
(Apr) 10:1A 1997
Background. SHR are a genetic strain of rat prone to the
development of hypertension by in part, activation of the
renin-angiotensin-aldosterone system (RAAS). Recent evidence
suggests
that relative nitric oxide (NO) synthase deficiency may also play
a
role in the hypertension found in this animal. This study pursued
a
possible link between activation of the RAAS and NO activity.
Study Results: 45 SHR rats were randomized to three groups
and
treated chronically with placebo, high-dose ramipril or low-dose
ramipril. After 21 months, the degree of LVH was assessed and
the amount of endothelium-induced relaxation was measured, as was
calcium ionophore-stimulated NO release. Superoxide production was
also determined.
The high-dose ramipril group of rats lived 36% longer than the
control
group, and had less LVH, better-preserved endothelial function,
increased NO production, and decreased superoxide production. The
responses appeared to be dose-related as they were intermediate in
the
low-dose ramipril group.
Comment: These observations are exciting, potentially
establishing a link between the RAAS and endothelial function / NO
production. Causality in terms of the RAAS axis can not be
confirmed
by this study, as rats in the high-dose ramipril group had the
lowest
blood pressures, and blood pressure per se may have been the cause
of
the changes found. Arlene Chapman, M.D., (University of
Colorado,
Denver)
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12th Annual ASH Meeting
H: Drug therapy :
ACE inhibitors