title: Predominant effect of A-type natriuretic peptide on reduction of oxidative stress during the treatment of patients with heart failure.
abstract: BACKGROUND
  Oxidative stress plays an important role in the pathogenesis of heart failure and was investigated in the present study of the role of exogenous A-type natriuretic peptide (ANP) in the patients with heart failure and in cultured neonatal rat cardiomyocytes.
  
  
  RESULTS
  The first protocol was to examine if an infusion of human ANP (carperitide) changed serum levels of TRX (thioredoxin) during the treatment of patients with heart failure compared with conventional therapy using furosemide. Protocol 2 investigated whether ANP had a direct antioxidant action on the failing heart by measuring TRX gene expression and reactive oxygen species (ROS) production in cultured neonatal rat cardiomyocytes. In Protocol 1, 8 patients were treated with only an intravenous bolus of furosemide and 11 patients with only an intravenous infusion of carperitide for 24 h. Serum TRX levels significantly decreased at 4 h (p<0.03) and at 24 h (p<0.05) in the carperitide group, whereas they decreased slightly but were not significantly different in the furosemide group. In Protocol 2, it was found that a low dose of exogenous ANP of 10(-9) mol/L significantly suppressed TRX expression and ROS production in cardiomyocytes.
  
  
  CONCLUSIONS
  Carperitide infusion has a predominantly antioxidant action, in addition to improving the hemodynamics of patients with acute heart failure. Furthermore, carperitide infusion should have a direct antioxidant effect on the failing heart.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Shono
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
authors.forename: Masafumi
authors.initials: M
authors.lastname: Nakayama
authors.forename: Megumi
authors.initials: M
authors.lastname: Yamamuro
authors.forename: Koji
authors.initials: K
authors.lastname: Abe
authors.forename: Satoru
authors.initials: S
authors.lastname: Suzuki
authors.forename: Yuji
authors.initials: Y
authors.lastname: Mizuno
authors.forename: Seigo
authors.initials: S
authors.lastname: Sugiyama
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Saito
authors.forename: Kazuwa
authors.initials: K
authors.lastname: Nakao
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Yasue
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
mesh_terms: D000368:Aged; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D009320:Atrial Natriuretic Factor / Q000494:pharmacology* / Q000627:therapeutic use*; D002303:Cardiac Output, Low / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D002478:Cells, Cultured; D004232:Diuretics / Q000494:pharmacology / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D005260:Female; D005665:Furosemide / Q000494:pharmacology / Q000627:therapeutic use; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013879:Thioredoxins / Q000235:genetics / Q000378:metabolism
chemical_list: D000975:Antioxidants; D004232:Diuretics; C472955:NPPA protein, human; D017382:Reactive Oxygen Species; D013879:Thioredoxins; D005665:Furosemide; D009320:Atrial Natriuretic Factor