MONDAY, Feb. 9, 2015 (HealthDay News) -- Different angiotensin receptor blockers (ARBs) have distinct potencies for suppressing adrenal β-arrestin1 (βarr1)-dependent post-myocardial infarction (MI) hyperaldosteronism, according to a letter published in the Dec. 30 issue of the Journal of the American College of Cardiology.
Anastasios Lymperopoulos, Ph.D., from the Nova Southeastern University College of Pharmacy in Fort Lauderdale, Fla., and colleagues examined the potencies of ARBs at suppression of adrenal βarr1-dependent post-MI hyperaldosteronism in an in vivo rat model.
The researchers found that in post-MI rats overexpressing βarr1 specifically in their adrenal glands, seven days of treatment with valsartan or candesartan correlated with reductions in circulating aldosterone levels; this translated into significantly improved cardiac function in terms of ejection fraction and isoproterenol-stimulated contractility. Irbesartan treatment did not reduce circulating aldosterone levels or prevent the decline in cardiac performance in these rats. Candesartan correlated with a significant reduction in post-MI cardiac fibrosis, while no effect was seen with irbesartan. Treatment with candesartan and valsartan correlated with a significant reduction in the adverse remodeling-associated biomarkers collagen I, atrial natriuretic peptide, and B-type natriuretic peptide, while there was no improvement in these markers with irbesartan.
"These pre-clinical findings strongly suggest that the pharmacological effects of the ARB drugs on adrenal angiotensin II type 1 receptor-activated βarr1 have to be taken into account when comparing their clinical effectiveness in heart disease (e.g., heart failure) treatment or when their propensity for developing the 'aldosterone breakthrough' phenomenon is considered," the authors write.
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