title: Cardiac atria are the primary source of ANP release in hypoxia-adapted rats.
abstract: OBJECTIVE
  atrial natriuretic peptide (ANP) is released from the heart in response to hypoxia and helps mitigate the development of pulmonary hypertension. However, the mechanism of hypoxia-induced ANP release is not clear. The cardiac atria are the primary source of ANP secretion under normal conditions, but right ventricular ANP expression is markedly up-regulated during adaptation to hypoxia. We sought to better understand mechanisms of cardiac ANP release during adaptation to hypoxia.
  
  
  METHODS
  we measured hypoxia-induced ANP release from isolated perfused rat hearts obtained from normoxia and hypoxia-adapted rats before and after removal of the atria.
  
  
  RESULTS
  in both normoxia- and hypoxia-adapted hearts, ANP levels in the perfusate increased within 15 min of hypoxia. Hypoxia-induced ANP release was greater from hypoxia-adapted than normoxia-adapted hearts. Baseline and hypoxia-induced ANP release were considerably greater with the atria intact (213±29 to 454±62 and 281±26 to 618±87 pg/ml for normoxia- and hypoxia-adapted hearts respectively, P<0.001 for both) than with atria removed (94±17 to 131±32 and 103±26 to 201±55 pg/ml, respectively, P<0.002 for both). Hypoxia-induced ANP release was reduced over 80% by removing the atria in both normoxia- and in hypoxia-adapted hearts. Acute hypoxia caused a transient increase in lactate release and reductions in pH and left ventricular generated force, but no differences in pH or left ventricular generated force were seen between normoxia- and hypoxia-adapted rats.
  
  
  CONCLUSIONS
  we conclude that the right ventricle is not a major source of cardiac ANP release in normoxia- or hypoxia-adapted rats.
authors.affiliation: Division of Pulmonary Medicine, Memorial Hospital of Rhode Island, Pawtucket, RI, United States.
authors.forename: Brian
authors.initials: B
authors.lastname: Casserly
authors.forename: Linda
authors.initials: L
authors.lastname: Pietras
authors.forename: Joy
authors.initials: J
authors.lastname: Schuyler
authors.forename: Richard
authors.initials: R
authors.lastname: Wang
authors.forename: Nicholas S
authors.initials: NS
authors.lastname: Hill
authors.forename: James R
authors.initials: JR
authors.lastname: Klinger
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D001835:Body Weight; D002118:Calcium / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006325:Heart Atria / Q000378:metabolism* / Q000601:surgery; D006863:Hydrogen-Ion Concentration; D017380:Hypertrophy, Right Ventricular / Q000473:pathology; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism; D010477:Perfusion; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology; D017725:Ventricular Pressure / Q000502:physiology
chemical_list: D019344:Lactic Acid; D009320:Atrial Natriuretic Factor; D012964:Sodium; D005947:Glucose; D011188:Potassium; D002118:Calcium