TY - JOUR
T1 - The influence of high versus low sodium intake on blood pressure and haemodynamics in patients with morbid obesity
AU - Bonfils, Peter K
AU - Taskiran, Mustafa
AU - Damgaard, Morten
AU - Goetze, Jens P
AU - Floyd, Andrea K
AU - Funch-Jensen, Peter
AU - Kristiansen, Viggo B
AU - Gadsbøll, Niels
PY - 2013/11
Y1 - 2013/11
N2 - 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.Method: 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 ±â€Š4%; obese, normotensive patients: 10 ±â€Š11%; nonobese controls: 7 ±â€Š6%), cardiac output (CO) (obese, hypertensive patients: 17 ±â €Š12%; obese, normotensive patients: 20 ±  16%; nonobese controls: 13 ±  14%) and stroke volume (SV) (obese, hypertensive patients: 27 ±â€Š26%; obese, normotensive patients: 27 ±â€Š24%; nonobese controls: 18 ±â€Š27%) 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 ±â€Š11%; obese, normotensive patients: - 10 ±â€Š12%; nonobese controls: -5 ±â€Š14%). 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.Conclusion: 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.
AB - 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.Method: 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 ±â€Š4%; obese, normotensive patients: 10 ±â€Š11%; nonobese controls: 7 ±â€Š6%), cardiac output (CO) (obese, hypertensive patients: 17 ±â €Š12%; obese, normotensive patients: 20 ±  16%; nonobese controls: 13 ±  14%) and stroke volume (SV) (obese, hypertensive patients: 27 ±â€Š26%; obese, normotensive patients: 27 ±â€Š24%; nonobese controls: 18 ±â€Š27%) 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 ±â€Š11%; obese, normotensive patients: - 10 ±â€Š12%; nonobese controls: -5 ±â€Š14%). 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.Conclusion: 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.
U2 - 10.1097/hjh.0b013e328363c769
DO - 10.1097/hjh.0b013e328363c769
M3 - Journal article
C2 - 23868085
SN - 0263-6352
VL - 31
SP - 2220-9; discussion 2229
JO - Journal of Hypertension
JF - Journal of Hypertension
IS - 11
ER -
