© 1996 American Heart Association, Inc.
Articles |
Altered Ventricular and Myocyte Response to Angiotensin II in Pacing-Induced Heart Failure
From the Section of Cardiology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC.
Correspondence to Che-Ping Cheng, MD, PhD, Section of Cardiology, Bowman Gray School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1045.
Abstract Alterations in the cardiac response to
angiotensin II (Ang II) may contribute to the functional
impairment in tachycardia-induced heart failure
(congestive heart failure [CHF]). Accordingly, we studied the
response to Ang II in eight conscious instrumented dogs before and
after inducing CHF. Left ventricular (LV)
performance was assessed by measuring LV pressure and LV
volume. Isolated myocyte function was evaluated using
computer-assessed videomicroscopy. In conscious animals before CHF,
Ang II produced a load-dependent slowing of the time constant of LV
relaxation (
) and did not depress intact LV contractile function.
After CHF, although Ang II produced a similar increase in LV
systolic pressure, the increases in LV diastolic
pressure and time constant were much greater, and contractile
performance was depressed. These changes persisted when the
elevation of end-systolic pressure was prevented by
nitroprusside. Similar changes were also present after autonomic
blockade. In isolated myocytes, before CHF, Ang II
(10-6 mol/L) produced a slight positive
inotropic effect. In contrast, after CHF, Ang II produced a negative
inotropic effect and slowed the rate of relengthening. The effects in
the intact LV and myocytes were reversed by an Ang II AT1
receptor blocker (losartan). We conclude that
pacing-induced CHF alters the LV and myocyte response to Ang II, so
that Ang II produces direct depressions in intact LV contraction,
relaxation, and filling and exacerbates myocyte contractile
dysfunction. These effects are mediated through the activation of
AT1 receptors.
Key Words: heart failure • contractility • relaxation • angiotensin II • isolated myocytes
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