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Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario, Canada K1Y 4W7
Mechanical stretch, ANG II, and
1-receptor stimulation may
contribute to cardiac remodeling after myocardial infarction (MI). Each
of these mechanisms involves different signaling pathways for the
cellular hypertrophic response. All three also activate the
Na+/H+
exchanger. In the present study we evaluated the hypothesis that activation of the
Na+/H+
exchanger is involved in parallel with other signaling mechanisms for
ANG II. Three days before coronary artery ligation, rats were randomly
allocated to no treatment or treatment with amiloride, losartan, or
amiloride and losartan in combination. Four weeks after coronary artery
ligation, left ventricular (LV) function was assessed from in vivo
resting cardiac pressures, hemodynamic responses to cardiac volume and
pressure load, and cardiac remodeling by in vitro pressure-volume
curves and LV and right ventricle (RV) weight. Amiloride and losartan
given alone to a similar extent attenuated the shift of the
pressure-volume curve to the right. This effect was significantly more
pronounced with amiloride and losartan in combination. Each drug alone
to a minor extent improved LV responses to pressure and volume load.
However, with amiloride and losartan in combination, close-to-normal
responses to pressure and volume load were observed. Losartan and
amiloride alone had only a small effect on development of RV
hypertrophy after MI but in combination completely prevented the RV
hypertrophy. Amiloride and losartan appear to be complementary in
prevention of cardiac remodeling and LV dysfunction after MI. This
finding suggests that, besides ANG II, other mechanisms activating the
Na+/H+
exchanger contribute to cardiac remodeling after MI.
amiloride; losartan; left ventricular remodeling; left ventricular failure
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