Reactivity to Norepinephrine and Effect of Sodium on Blood Pressure During Weight Loss
- Fagerberg, Björn
- Andersson, Ove K.
- Persson, Bengt
- Hedner, Thomas
SUMMARY
Eighteen moderately obese middle-aged men with untreated mild hypertension were randomized to two groups and placed on a low energy diet regimen for 9 to 11 weeks. In Group 1 (n= 10) the amount of sodium chloride in the diet maintained the urinary sodium excretion at the predieting level. Mean body mass was reduced by 9.1 ± 0.7 (sem) kg. Mean intra-arterial pressure showed no significant change. There were significant decreases in heart rate (p< 0.05) and urinary norepinephrine excretion (p< 0.05) but not in plasma concentration of norepinephrine. In Group II (n= 8) energy as well as sodium intake was restricted, with a 95 ± 22 mmol/24 hour reduction of urinary sodium excretion. Rody mass decreased by 9.3 ± 1.1 kg, and mean arterial pressure decreased by −18.9 to −4.3 mm Hg (95¶ confidence interval). There were also significant reductions in heart rate (p< 0.001) and plasma norepinephrine concentrations (p< 0.01) but not in urinary norepinephrine excretion. The pressor response (mean arterial pressure) to norepinephrine infusion at different dose rates was significantly elevated (p< 0.05) in Group I during dieting in comparison with baseline. The blood pressure response to norepinephrine during dieting in patients in Group II was not changed from baseline. The difference in blood pressure response to norepinephrine cannot be explained by changes in clearance rates and plasma volumes. The results indicate that the lack of hypotensive response observed in patients on moderate energy restriction with unchanged sodium intake might have been caused by increased vascular reactivity to norepinephrine. Although sympathetic vasoconstrictor tone was reduced, increased vascular reactivity may have kept the blood pressure level unchanged. Blood pressure fell in patients on combined energy and sodium restriction as the lowered sympathetic nervous activity was not offset by an increase in reactivity.
(Hypertension 7: 586-592, 1985)