title: Effects of sodium intake on plasma potassium and renin angiotensin aldosterone system in conscious dogs.
abstract: OBJECTIVE
  The operating range of the renin-angiotensin-aldosterone system is ill-defined. This study quantifies renin-angiotensin-aldosterone system activity as a function of sodium intake.
  
  
  METHODS
  Renin-angiotensin-aldosterone system variables were measured daily after a sudden reduction in sodium intake (3.0-0.5 mmol kg(-1) day(-1)) or at steady states generated by eight levels of sodium intake (0.5-8.0 mmol kg(-1) day(-1)). Potassium intake was 2.79 +/- 0.03 mmol kg(-1) day(-1). Arterial blood pressure was measured invasively. Hormone concentrations were determined by radioimmunoassays. Glomerular filtration rate and plasma volume were determined by standard methods.
  
  
  RESULTS
  Sudden sodium intake reduction doubled plasma renin activity and angiotensin II, and tripled aldosterone on day 1 with only small non-significant additional changes on the following days. Different levels of sodium intake did not affect arterial blood pressure, heart rate, and plasma concentrations of sodium, angiotensinogen, atrial natriuretic peptide, vasopressin, glomerular filtration rate and diuresis. With increasing sodium intake, plasma volume increased by 0.47 +/- 0.04 mL (kg body mass)(-1) (unit increase in Na intake)(-1) (P < 0.01), and plasma potassium decreased with the slope -0.038 mm [(mmol Na+ intake) (kg body mass)(-1) day(-1)](-1) (P = 0.001) while plasma renin-activity, angiotensin II, and aldosterone decreased systematically as expected.
  
  
  CONCLUSIONS
  A step reduction in sodium intake alters renin-angiotensin-aldosterone system activity on day 1 with little further change the subsequent 4 days. Week-long increases in sodium intake decreases renin-angiotensin-aldosterone system activity, increases plasma volume, and decreases plasma potassium. Isolated decreases in sodium intake increase aldosterone secretion via volume-mediated action on the renin-angiotensin system and via increases in plasma potassium.
authors.affiliation: Department of Physiology and Pharmacology, Institute of Medical Biology, University of Southern Denmark, Odense, Denmark.
authors.forename: M J
authors.initials: MJ
authors.lastname: Kjolby
authors.forename: E
authors.initials: E
authors.lastname: Kompanowska-Jezierska
authors.forename: S
authors.initials: S
authors.lastname: Wamberg
authors.forename: P
authors.initials: P
authors.lastname: Bie
mesh_terms: D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000808:Angiotensinogen / Q000097:blood; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D004231:Diuresis / Q000502:physiology; D004285:Dogs; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D010953:Plasma Volume / Q000502:physiology; D011188:Potassium / Q000097:blood*; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology*; D012964:Sodium / Q000008:administration & dosage* / Q000097:blood; D014667:Vasopressins / Q000097:blood
chemical_list: D014667:Vasopressins; D000808:Angiotensinogen; D000804:Angiotensin II; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium; D012083:Renin; D011188:Potassium