Rosiglitazone improves the natriuretic response to atrial natriuretic peptide in rats with experimental congestive heart failure: possible involvement of a post-guanylate cyclase mechanism

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.