Key Points
- To evaluate changes in angiotensin II AT1a, AT1b, and AT2 receptor gene expression in rat left ventricles subjected to pressure overload and subsequent pharmacological therapy.
- Induced left ventricular pressure overload hypertrophy in rats via aortic banding for 6 weeks.
- Treated banded rats with the AT1 receptor antagonist losartan (40 mg/kg) or vehicle control for 6 additional weeks alongside sham-operated controls.
- Quantified left ventricular weight, AT1a, AT1b, and AT2 receptor mRNA, beta-myosin:alpha-myosin mRNA ratios, and atrial natriuretic peptide mRNA levels.
- Aortic banding increased relative left ventricular weight from 1.73 ± 0.06 to 2.81 ± 0.25 g/kg, shifted the beta-myosin:alpha-myosin mRNA ratio from 0.30 ± 0.02 to 1.94 ± 0.55, and raised atrial natriuretic peptide mRNA 18-fold.
- Losartan treatment ameliorated hypertrophy, yielding relative heart weights of 2.39 ± 0.14 g/kg, a myosin ratio of 1.04 ± 0.20, and a blunted 11-fold rise in atrial natriuretic peptide mRNA.
- Levels of AT1a, AT1b (present at a 5:1 relative ratio), and AT2 receptor mRNA remained unaltered across hypertrophied, losartan-treated, and control left ventricles.
Structured PICO
Does losartan alter angiotensin II receptor gene expression in rats with left ventricular hypertrophy induced by aortic banding?
PPopulationRats subjected to ventricular pressure overloading induced by aortic banding for 6 weeks
IInterventionLosartan (40 mg/kg) for 6 weeks after banding
CComparatorVehicle-treated or sham-treated controls
OOutcomeExpression of angiotensin II AT1a, AT1b and AT2 receptor genes in the left ventriclessurrogate
In a rat model of pressure overload-induced left ventricular hypertrophy, losartan ameliorated hypertrophy without altering the expression levels of angiotensin II AT1a, AT1b, and AT2 receptor genes.