title: The influence of high versus low sodium intake on blood pressure and haemodynamics in patients with morbid obesity.
abstract: BACKGROUND
  Many patients with morbid obesity (BMI > 40 kg/m) have hypertension. The complex pathophysiological abnormalities linking hypertension to obesity have not been fully clarified, but abnormal sodium handling could be an important mechanism.
  
  
  METHODS
  Therefore, we examined changes in body fluid compartments and haemodynamic responses (at rest and during exercise) after 5 days of a low-sodium diet (90 mmol/day) and 5 days of a high-sodium diet (250 mmol/day) in 12 morbidly obese, hypertensive patients; 12 morbidly obese, normotensive patients and 12 nonobese controls.
  
  
  RESULTS
  High sodium intake as compared to low sodium intake was associated with an increase in plasma volume (obese, hypertensive patients: 5 ± 4%; obese, normotensive patients: 10 ± 11%; nonobese controls: 7 ± 6%), cardiac output (CO) (obese, hypertensive patients: 17 ± 12%; obese, normotensive patients: 20 ± 16%; nonobese controls: 13 ± 14%) and stroke volume (SV) (obese, hypertensive patients: 27 ± 26%; obese, normotensive patients: 27 ± 24%; nonobese controls: 18 ± 27%) in all three groups with no differences between the groups. Despite an increase in CO during high salt intake, 24-h blood pressure (BP) was unchanged in patients and controls as a result of a reduction in total peripheral resistance (obese, hypertensive patients: -11 ± 11%; obese, normotensive patients: -10 ± 12%; nonobese controls: -5 ± 14%). Similar changes were observed during an incremental bicycle exercise test wherein CO and SV were higher, whereas mean arterial BP was unchanged at each exercise level during high sodium intake.
  
  
  CONCLUSIONS
  Despite substantial increases in CO and SV, we did not observe any significant change in BP during high sodium intake, neither in morbid obese patients nor in lean individuals.
authors.affiliation: aDepartment of Clinical Physiology and Nuclear Medicine bDepartment of Medicine, Koege Hospital, University of Copenhagen cDepartment of Clinical Biochemistry, Rigshospitalet dDepartment of Surgery, Division of Bariatric Surgery, Koege Hospital, University of Copenhagen, Copenhagen eDepartment of Bariatric Surgery, Aleris-Hamlet and Clinical Institute, University of Aarhus, Aarhus fDepartment of Surgical Gastroenterology, Hvidovre Hospital, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Peter K
authors.initials: PK
authors.lastname: Bonfils
authors.forename: Mustafa
authors.initials: M
authors.lastname: Taskiran
authors.forename: Morten
authors.initials: M
authors.lastname: Damgaard
authors.forename: Jens P
authors.initials: JP
authors.lastname: Goetze
authors.forename: Andrea K
authors.initials: AK
authors.lastname: Floyd
authors.forename: Peter
authors.initials: P
authors.lastname: Funch-Jensen
authors.forename: Viggo B
authors.initials: VB
authors.lastname: Kristiansen
authors.forename: Niels
authors.initials: N
authors.lastname: Gadsbøll
mesh_terms: D001794:Blood Pressure / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology; D004039:Diet, Sodium-Restricted; D015444:Exercise / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D009767:Obesity, Morbid / Q000150:complications / Q000503:physiopathology*; D012146:Rest / Q000502:physiology; D012982:Sodium, Dietary / Q000008:administration & dosage*; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D012982:Sodium, Dietary