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These side effects are attributed in part to direct salt\u2010retaining effect of TZD<\/jats:styled-content>s at the renal collecting duct. A recent study from our group revealed that prolonged rosiglitazone (RGZ<\/jats:styled-content>) treatment caused no Na+\/H2<\/jats:sub>O retention or up\u2010regulation of Na+<\/jats:sup> transport\u2010linked channels\/transporters in experimental congestive heart failure (CHF<\/jats:styled-content>) induced by surgical aorto\u2010caval fistula (ACF<\/jats:styled-content>). The present study examines the effects of RGZ<\/jats:styled-content> on renal and cardiac responses to atrial natriuretic peptide (ANP<\/jats:styled-content>), Acetylcholine (Ach) and S\u2010Nitroso\u2010N<\/jats:italic>\u2010acetylpenicillamine (SNAP<\/jats:styled-content>\u2010NO<\/jats:styled-content> donor). Furthermore, we assessed the impact of RGZ<\/jats:styled-content> on gene expression related to the ANP<\/jats:styled-content> signalling pathway in animals with ACF<\/jats:styled-content>. Rats subjected to ACF<\/jats:styled-content> (or sham) were treated with either RGZ<\/jats:styled-content> (30\u00a0mg\/kg\/day) or vehicle for 4\u00a0weeks. Cardiac chambers pressures and volumes were assessed invasively via Miller catheter. Kidney excretory and renal hemodynamic in response to ANP<\/jats:styled-content>, Ach and SNAP<\/jats:styled-content> were examined. Renal clearance along with cyclic guanosine monophosphate (cGMP<\/jats:styled-content>), gene expression of renal CHF<\/jats:styled-content>\u2010related genes and ANP<\/jats:styled-content> signalling in the kidney were determined. RGZ<\/jats:styled-content>\u2010treated CHF<\/jats:styled-content> rats exhibited significant improvement in the natriuretic responses to ANP<\/jats:styled-content> infusion. This \u2018sensitization\u2019 to ANP<\/jats:styled-content> was not associated with increases in neither urinary cGMP<\/jats:styled-content> nor in vitro cGMP<\/jats:styled-content> production. However, RGZ<\/jats:styled-content> caused down\u2010regulation of several genes in the renal cortex (Ace, Nos3 and Npr1) and up\u2010regulation of ACE<\/jats:styled-content>2, Agtrla, Mme and Cftr along down\u2010regulation of Avpr2, Npr1,2, Nos3 and Pde3 in the medulla. In conclusion, CHF<\/jats:styled-content>+RGZ<\/jats:styled-content> rats exhibited significant enhancement in the natriuretic responses to ANP<\/jats:styled-content> infusion, which are known to be blunted in CHF<\/jats:styled-content>. This \u2018sensitization\u2019 to ANP<\/jats:styled-content> is independent of cGMP<\/jats:styled-content> signalling, yet may involve post\u2010cGMP<\/jats:styled-content> signalling target genes such as ACE<\/jats:styled-content>2, CFTR<\/jats:styled-content> and V2 receptor. The possibility that TZD<\/jats:styled-content> treatment in uncomplicated CHF<\/jats:styled-content> may be less detrimental than thought before deserves additional investigations.<\/jats:p>","DOI":"10.1111\/jcmm.14366","type":"journal-article","created":{"date-parts":[[2019,5,14]],"date-time":"2019-05-14T05:59:36Z","timestamp":1557813576000},"page":"4779-4794","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Rosiglitazone treatment restores renal responsiveness to atrial natriuretic peptide in rats with congestive heart failure"],"prefix":"10.1111","volume":"23","author":[{"given":"Ilia","family":"Goltsman","sequence":"first","affiliation":[{"name":"Department of Physiology Bruce Rappaport Faculty of Medicine Technion\u2010IIT Haifa Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emad E.","family":"Khoury","sequence":"additional","affiliation":[{"name":"Department of Physiology Bruce 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