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Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario K1Y 4W7, Canada
To assess the possible
contribution of the circulatory and cardiac renin-angiotensin system
(RAS) to the cardiac hypertrophy induced by a 
-agonist, the present
study evaluated the effects of isoproterenol, alone or combined with an
angiotensin I-converting enzyme inhibitor or AT1 receptor
blocker, on plasma and LV renin activity, ANG I, and ANG II, as well as
left ventricular (LV) and right ventricular (RV) weight. Male Wistar
rats received isoproterenol by osmotic minipump subcutaneously and
quinapril or losartan once daily by gavage. Plasma and LV ANGs were
measured by radioimmunoassay after separation by HPLC. Isoproterenol
alone decreased blood pressure, more markedly when combined with
losartan or quinapril. Isoproterenol significantly increased LV and RV
weight and total collagen. Neither losartan nor quinapril inhibited the
increases in LV or RV weight. Losartan prevented the increase in RV
collagen but enhanced the increase in LV collagen. Isoproterenol
increased plasma renin, ANG I, and ANG II three- to fourfold.
Isoproterenol combined with losartan or quinapril, caused marked
further increases except for a significant decrease in plasma ANG II
with quinapril. Isoproterenol alone did not increase LV ANG II
and, combined with losartan or quinapril, actually decreased LV ANG II.
These results indicate that isoproterenol-induced cardiac hypertrophy
is associated with clear increases in plasma ANG II, but not in LV ANG
II. Both losartan and quinapril lower LV ANG II below control levels,
but do not prevent the isoproterenol-induced cardiac hypertrophy. These
findings do not support a role for the circulatory or cardiac RAS in
the cardiac trophic responses to -receptor stimulation.
-agonist; angiotensin II; heart; angiotensin I-converting
enzyeme inhibitor; AT1-receptor blocker
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