首页> 外文期刊>International Journal of Hypertension >The Effects of Salt and Glucose Intake on Angiotensin II and Aldosterone in Obese and Nonobese Patients with Essential Hypertension
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The Effects of Salt and Glucose Intake on Angiotensin II and Aldosterone in Obese and Nonobese Patients with Essential Hypertension

机译:盐酸葡萄糖摄入对血管紧张素II和醛固酮在肥胖和非血管基因高血压患者中的影响

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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/m2) (11 patients and 8 control) and nonobese (BMI 30?Kg/m2) (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.
机译:背景。尚不清楚地知道原发性高血压的确切机制。脂肪组织中的肾素 - 血管紧张素 - 醛固酮系统(RAA)的活化可代表肥胖和高血压之间的重要联系。本研究调查了口服摄入葡萄糖的影响和不含NaC1对血管紧张素II(Angii)和aldosterone在肥胖和非必需高血压患者中的血管紧张素和醛固酮的影响。方法。研究了二十名新诊断的未经治疗的必需高血压患者和15次与年龄,性别和BMI匹配的15个正常控制受试者。参与者禁食过夜(8-10?HRS),然后每次受试者单独服用75克(GM NaCl),每次溶解在250μlmL中。监测受试者2小时。测量半小时BP,血浆葡萄糖(PG),血清Na +,K +,胰岛素,AngiI和醛固酮。将受试者分为肥胖(BMI> 30?KG / M2)(11名患者和8次对照)和非同源(BMI <30 kg / M2)(9例和7名患者)。结果。用NaCl血清摄入葡萄糖后,与非同源患者相比,肥胖高血压患者的Angii显着高(P = 0.016)。与非同源患者Na相比,肥胖高血压患者中,葡萄糖的摄入量导致肥胖患者中显着更高的血清NA(p = 0.009)。肥胖患者血清醛固酮(P = 0.03,葡萄糖后)显着较高;与其相应的正常控制受试者相比,葡萄糖后的葡萄糖葡萄糖后,葡萄糖葡萄糖葡萄糖)和非同源患者(P = 0.000和P = 0.000)。在肥胖和非同源患者中,葡萄糖和NaCl的摄入量显示出血清Angii和醛固酮水平没有显着变化,其在肥胖患者中血清NA的显着增加(p = 0.03)和血清K的显着减少在非患者中(p = 0.001)。结论。通过用NaCl摄入葡萄糖,抑制抑制或对血管腺系分泌的不恰当的维护可能表明可能的原发性高血压的可能机制。

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