We measured plasma and platelet magnesium concentrations, plasma epinephrine and norepinephrine, and plasma aldosterone and renin concentrations in normotensive (NT-Ob, n = 19, BMI 35.7 +/- 7.4 kg/m2, WHR 0.92 +/- 0.05) and hypertensive (HT-Ob, n = 11, BMI 35.2 +/- 3.6 kg/m2, WHR 0.93 +/- 0.07) obese subjects, and in a group of age- and sex-matched lean controls (n = 14, BMI 23.1 +/- 1.8 kg/m2, WHR 0.79 +/- 0.05). Plasma aldosterone and renin concentrations were significantly higher in obese subjects with respect to controls. Moreover, plasma norepinephrine and epinephrine levels were significantly increased in obese subjects, and plasma norepinephrine was higher in HT-Ob when compared to NT-Ob group. Platelet magnesium concentrations were significantly reduced in both normotensive and hypertensive obese subjects with respect to controls (controls 2.65 +/- 0.35 mumol/10(8) cells, NT-Ob 2.02 +/- 0.19 mumol/10(8) cells--p < 0.001, HT-Ob 1.98 +/- 0.18 mumol/10(8) cells--p < 0.001), while a slightly significant decrease in plasma magnesium levels was only detectable in HT-Ob group. Urinary magnesium and magnesium fractional excretion were significantly increased in hypertensive obeses. Pearson's correlation analysis, separately performed in each group of subjects, showed that plasma aldosterone, renin, epinephrine, norepinephrine and magnesium fractional excretion were negatively correlated to platelet magnesium levels in NT-Ob and HT-Ob groups, but not in lean controls. The multiple linear regression analysis performed in the whole group of obese subjects considering platelet magnesium as a dependent variable showed that platelet magnesium decrease together with the increase in plasma epinephrine (p = 0.046) and norepinephrine (p = 0.020), also after adjusting for age, sex, BMI, WHR, HOMA IR and diagnosis of hypertension. Furthermore, platelet magnesium showed a trend for negative association (p < 0.1) to plasma aldosterone and magnesium fractional excretion in multivariate analysis. The impairment in platelet magnesium handling observed in normotensive and hypertensive obese patients seems to be associated to a rise in renin-angiotensin-aldosterone and sympathetic systems activity. Our results suggest that platelet magnesium depletion, together with disturbances of salt-regulating hormones and catecholamines, may be involved in the pathophysiology of cardiovascular complications from obesity.

Platelet magnesium depletion in normotensive and hypertensive obese subjects: the role of salt-regulating hormones and catecholamines.

CORICA, Francesco;BUEMI, Michele;NICITA MAURO, Vittorio;MACAIONE, Salvatore;IENTILE, Riccardo
1999-01-01

Abstract

We measured plasma and platelet magnesium concentrations, plasma epinephrine and norepinephrine, and plasma aldosterone and renin concentrations in normotensive (NT-Ob, n = 19, BMI 35.7 +/- 7.4 kg/m2, WHR 0.92 +/- 0.05) and hypertensive (HT-Ob, n = 11, BMI 35.2 +/- 3.6 kg/m2, WHR 0.93 +/- 0.07) obese subjects, and in a group of age- and sex-matched lean controls (n = 14, BMI 23.1 +/- 1.8 kg/m2, WHR 0.79 +/- 0.05). Plasma aldosterone and renin concentrations were significantly higher in obese subjects with respect to controls. Moreover, plasma norepinephrine and epinephrine levels were significantly increased in obese subjects, and plasma norepinephrine was higher in HT-Ob when compared to NT-Ob group. Platelet magnesium concentrations were significantly reduced in both normotensive and hypertensive obese subjects with respect to controls (controls 2.65 +/- 0.35 mumol/10(8) cells, NT-Ob 2.02 +/- 0.19 mumol/10(8) cells--p < 0.001, HT-Ob 1.98 +/- 0.18 mumol/10(8) cells--p < 0.001), while a slightly significant decrease in plasma magnesium levels was only detectable in HT-Ob group. Urinary magnesium and magnesium fractional excretion were significantly increased in hypertensive obeses. Pearson's correlation analysis, separately performed in each group of subjects, showed that plasma aldosterone, renin, epinephrine, norepinephrine and magnesium fractional excretion were negatively correlated to platelet magnesium levels in NT-Ob and HT-Ob groups, but not in lean controls. The multiple linear regression analysis performed in the whole group of obese subjects considering platelet magnesium as a dependent variable showed that platelet magnesium decrease together with the increase in plasma epinephrine (p = 0.046) and norepinephrine (p = 0.020), also after adjusting for age, sex, BMI, WHR, HOMA IR and diagnosis of hypertension. Furthermore, platelet magnesium showed a trend for negative association (p < 0.1) to plasma aldosterone and magnesium fractional excretion in multivariate analysis. The impairment in platelet magnesium handling observed in normotensive and hypertensive obese patients seems to be associated to a rise in renin-angiotensin-aldosterone and sympathetic systems activity. Our results suggest that platelet magnesium depletion, together with disturbances of salt-regulating hormones and catecholamines, may be involved in the pathophysiology of cardiovascular complications from obesity.
1999
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/1892385
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