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

We measured plasma and platelet magnesium concentrations, plasma epinephrin e and norepinephrine, and plasma aldosterone and renin concentrations in no rmotensive (NT-Ob, n = 19, BMI 35.7 +/- 7.4 kg/m(2), WHR 0.92 +/- 0.05) and hypertensive (HT-Ob, n = 11, BMI 35.2 +/- 3.6 kg/m(2), WHR 0.93 +/- 0.07) obese subjects, and in a group of age- and sex-matched lean controls (n = 1 4, BMI 23.1 +/- 1.8 kg/m(2), WHR 0.79 +/- 0.051. Plasma aldosterone and ren in concentrations were significantly higher in obese subjects with respect to controls. Moreover, plasma norepinephrine and epinephrine levels were si gnificantly increased in obese subjects, and plasma norepinephrine was high er in HT-Ob when compared to NT-Ob group. Platelet magnesium concentrations were significantly reduced in both normotensive and hypertensive obese sub jects with respect to controls (controls 2.65 +/- 0.35 mu mol/10(8) cells, NT-Ob 2.02 +/- 0.19 mu mol/10(8) cells - p < 0.001, HT-Ob 1.98 +/- 0.18 mu mol/10(8) cells - p < 0.001), while a slightly significant decrease in plas ma magnesium levels was only detectable in HT-Ob group. Urinary magnesium a nd magnesium fractional excretion were significantly increased in hypertens ive obeses. Pearson's correlation analysis, separately performed in each gr oup of subjects, showed that plasma aldosterone, renin, epinephrine, norepi nephrine and magnesium fractional excretion were negatively correlated to p latelet magnesium levels in NT-Ob and HT-Ob groups, but not in lean control s. The multiple linear regression analysis performed in the whole group of obese subjects considering platelet magnesium as a dependent variable showe d that platelet magnesium decrease together with the increase in plasma epi nephrine (p = 0.046) and norepinephrine (p = 0.020), also after adjusting f or age, sex, BMI, WHR, HOMA IR and diagnosis of hypertension. Furthermore, platelet magnesium showed a trend for negative association (p < 0.1) to pla sma aldosterone and magnesium fractional excretion in multivariate analysis . The impairment in platelet magnesium handling observed in normotensive an d hypertensive obese patients seems to be associated to a rise in renin-ang iotensin-aldosterone and sympathetic systems activity. Our results suggest that platelet magnesium depletion, together with disturbances of salt-regul ating hormones and catecholamines, may be involved in the pathophysiology o f cardiovascular complications from obesity.