Why the study?
Does rosiglitazone improve the natriuretic response to atrial natriuretic peptide in rats with experimental congestive heart failure?
Does rosiglitazone improve the natriuretic response to atrial natriuretic peptide in rats with experimental congestive heart failure?
In rats with experimental CHF, chronic rosiglitazone treatment enhances renal ANP-induced natriuresis, likely via a post-guanylate cyclase mechanism.
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Hypothesis-generating for rosiglitazone in experimental CHF; should not change clinical practice.
Background Congestive heart failure (CHF) in patients and experimental animals is characterized by renal retention of salt and water and a blunted natriuretic/diuretic response to atrial natriuretic peptide (ANP). Recently, we reported that chronic treatment with the PPARgagonist rosiglitazone (RGZ) improved the natriuretic and diuretic responses to extracellular fluid volume expansion in rats with aorto-caval fistula, an experimental model of volume-overload CHF [1]. In the present study we explored whether RGZ improves also the natriuretic/diuretic response to ANP in rats with experimental CHF. In addition, we evaluated the effects of the drug on ANP-mediated cGMP signalling in the kidney.
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Goltsman et al. (2011) studied this question.
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