Central obesity and hypertension: pathophysiologic role of renal haemodynamics and function

OBJECTIVE: To investigate the role of alterations in renal haemodynamics and function and in plasma renin activity on obesity-induced hypertension. DESIGN: Renal haemodynamics and function, salt-regulating hormones and structural cardiac parameters were evaluated in 20 lean normotensives and in 64 obese subjects with central or peripheral fat distribution, 43 of them were normotensives and 21 of them were hypertensives. Obesity and central fat distribution were defined according to sex-specific 85th percentile respectively of Body Mass Index (BMI) and Waist to Hip Ratio (WHR). MEASUREMENTS: Serum immunoreactive insulin (IRI), plasma renin activity (PRA), plasma aldosterone (PA), microalbuminuria (UAE) and 24h urinary excretion of sodium (NaU) were evaluated by current methods. Renal haemodynamics was evaluated by radionuclide study according to Schlegel's and Gate's methods. By radionuclide study, effective renal plasma flow (ERPF), effective renal blood flow (ERBF), glomerular filtration rate (GFR), filtration fraction (FF) and renal vascular resistances (RVR) were measured. Left ventricular mass (LVM) and indexed for body height (LVM/H), cardiac output (CO) and total peripheral resistances (TPR) by ecocardiography were also calculated. RESULTS: CO, LVM and LVM/H were significantly (P < 0.05) higher in all the obese groups than lean controls. In addition, LVM and LVM/H were significantly (P < 0.05) higher in obese hypertensives than obese normotensives either with central fat distribution. TPR values were significantly (P < 0.05) higher in central obese hypertensives than peripheral obese hypertensives and than central obese normotensives. Moreover, IRI levels were significantly (P < 0.05) higher in central normotensive and hypertensive obese subjects than lean subjects. ERBF and ERPF were significantly (P < 0.05) lower and PRA levels were significantly higher only in central obese than lean subjects. On the contrary RVR were significantly (P < 0.05) higher in both obese hypertensive groups and in central obese normotensives than lean subjects. Comparisons between peripheral and central obese groups indicated that PRA, RVR and UAE were significantly (P < 0.05) higher and ERBF and ERPF values were significantly (P < 0.05) lower in both central obese groups than comparable subjects with peripheral obesity. Multiple regression analysis indicated that RVR increased significantly (P < 0.05) with WHR and PRA but not with CO and IRI. CONCLUSIONS: Our results indicate that obesity with body fat distribution of central type, more than obesity of peripheral type, is associated to abnormalities in renal haemodynamics and function. These data are consistent with the indication that change in renal haemodynamics take place at an early stage in the obesity-induced hypertension.