Abstract
BACKGROUND: The exact mechanisms for the development of essential hypertension are not known. Activation of the renin-angiotensin-aldosterone system (RAAS) in adipose tissue may represent an important link between obesity and hypertension. This study investigates the effects of oral intake of glucose with and without NaCl on angiotensin II (AngII) and aldosterone in obese and nonobese patients with essential hypertension. METHODS: Twenty newly diagnosed untreated essential hypertensive patients and 15 normotensive control subjects matched for age, gender, and BMI were studied. Participants fasted overnight (8-10 hrs), and then each subject took 75 gm glucose alone and with 3 gm NaCl, each dissolved in 250 ml. Subjects were monitored for 2 hours. Half hourly BP, plasma glucose (PG), serum Na(+), K(+), insulin, AngII, and aldosterone were measured. Subjects were classified into obese (BMI >30 Kg/m(2)) (11 patients and 8 control) and nonobese (BMI <30 Kg/m(2)) (9 patients and 7 control). RESULTS: After intake of glucose with NaCl serum, AngII was significantly higher in obese hypertensive patients compared with nonobese patients (P = 0.016). Intake of glucose with NaCl resulted in a significantly higher serum Na in obese hypertensive patients compared with nonobese patients Na (P = 0.009). Serum aldosterone was significantly higher in obese patients (P = 0.03, after glucose; P = 0.003, after glucose with NaCl) and in nonobese patients (P = 0.000 and P = 0.000, respectively) compared with their respective normotensive control subjects. In obese and nonobese patients, intake of glucose and glucose with NaCl showed no significant change in the levels of serum AngII and aldosterone which was associated a significant increase in serum Na in obese patients (P = 0.03) and a highly significant reduction in serum K in nonobese patients (P = 0.001). CONCLUSION: Failure of suppression or inappropriate maintenance of secretion of AngII and aldosterone in both hypertensive groups by intake of glucose with NaCl may indicate a possible mechanism of essential hypertension.