title: Catabolism of adenine nucleotides favors adenosine production following exercise in patients with chronic heart failure.
abstract: BACKGROUND
  Adenosine 5'-triphosphate is catabolized to adenosine 5'-monophosphate (AMP), which is further degraded by 2 pathways: deamination to inosine 5'-monophosphate and ammonia by AMP deaminase, or dephosphorylation to adenosine and inorganic phosphate by 5'-nucleotidase. Because adenosine is believed to be cardioprotective and we have reported that ammonia production decreased after exercise in patients with chronic heart failure (CHF), we determined if plasma adenosine levels after exercise increases in patients with CHF.
  
  
  RESULTS
  Maximal ergometer exercise tests with expired gas analysis were performed in 51 patients with CHF (age = 61 +/- 2 years, New York Heart Association [NYHA] class I/II/III = 19/18/14) and 20 age-matched normal controls. Serial changes in both plasma ammonia and adenosine levels were determined. The ratio for delta ammonia to peak work rate became smaller (control, NYHA I/II/III: 0.59 +/- 0.13/0.41 +/- 0.06/0.37 +/- 0.10/0.22 +/- 0.11 microg/dL x watts, respectively) and the ratio for delta adenosine to peak work rate was significantly higher in class III CHF (control, NYHA I/II/III: 0.93 +/- 0.21/0.86 +/- 0.14/1.11 +/- 0.27/2.92 +/- 0.67 nmol/L x watts, respectively).
  
  
  CONCLUSIONS
  In patients with CHF after exercise, the plasma levels of adenosine increased along with the decrease in the plasma levels of ammonia. Considering the physiologic cardioprotective actions of adenosine, the enhanced adenosine production after exercise may be an important adaptive response in patients with CHF.
authors.affiliation: Department of Cardiovascular Medicine, Faculty of Medicine, Graduate School of Medicine, Tottori University, Yonago, Japan.
authors.forename: Toru
authors.initials: T
authors.lastname: Kinugawa
authors.forename: Masashi
authors.initials: M
authors.lastname: Fujita
authors.forename: Kazuhide
authors.initials: K
authors.lastname: Ogino
authors.forename: Masahiko
authors.initials: M
authors.lastname: Kato
authors.forename: Shuichi
authors.initials: S
authors.lastname: Osaki
authors.forename: Osamu
authors.initials: O
authors.lastname: Igawa
authors.forename: Chiaki
authors.initials: C
authors.lastname: Shigemasa
authors.forename: Ichiro
authors.initials: I
authors.lastname: Hisatome
authors.forename: Masafumi
authors.initials: M
authors.lastname: Kitakaze
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism*; D000241:Adenosine / Q000096:biosynthesis* / Q000097:blood; D000368:Aged; D000641:Ammonia / Q000097:blood; D001794:Blood Pressure; D002303:Cardiac Output, Low / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D002316:Cardiotonic Agents / Q000097:blood / Q000378:metabolism*; D002908:Chronic Disease; D015444:Exercise; D005260:Female; D006321:Heart / Q000503:physiopathology; D006339:Heart Rate; D006801:Humans; D019271:Hypoxanthine / Q000097:blood; D008168:Lung / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption
chemical_list: D000227:Adenine Nucleotides; D002316:Cardiotonic Agents; D019271:Hypoxanthine; D000641:Ammonia; D000241:Adenosine