Alaagib Nouralsalhin, Sukkar Mohammed, Kardash Mohammed
Department of Physiology, Faculty of Medicine, University of Khartoum, Khartoum, Sudan.
Faculty of Medicine, Nile University, Khartoum, Sudan.
Int J Hypertens. 2020 Mar 19;2020:6017105. doi: 10.1155/2020/6017105. eCollection 2020.
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.
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) (11 patients and 8 control) and nonobese (BMI <30 Kg/m) (9 patients and 7 control).
After intake of glucose with NaCl serum, AngII was significantly higher in obese hypertensive patients compared with nonobese patients ( = 0.016). Intake of glucose with NaCl resulted in a significantly higher serum Na in obese hypertensive patients compared with nonobese patients Na ( = 0.009). Serum aldosterone was significantly higher in obese patients ( = 0.03, after glucose; = 0.003, after glucose with NaCl) and in nonobese patients ( = 0.000 and = 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 ( = 0.03) and a highly significant reduction in serum K in nonobese patients ( = 0.001).
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.
原发性高血压的确切发病机制尚不清楚。脂肪组织中肾素-血管紧张素-醛固酮系统（RAAS）的激活可能是肥胖与高血压之间的重要联系。本研究调查了肥胖和非肥胖原发性高血压患者口服葡萄糖加或不加氯化钠对血管紧张素II（AngII）和醛固酮的影响。
研究对象为20例新诊断的未经治疗的原发性高血压患者和15例年龄、性别和BMI相匹配的血压正常对照者。参与者禁食过夜（8 - 10小时），然后每位受试者单独服用75克葡萄糖以及葡萄糖加3克氯化钠，每种均溶解于250毫升水中。对受试者进行2小时监测。每半小时测量血压、血浆葡萄糖（PG）、血清钠、钾、胰岛素、AngII和醛固酮。受试者分为肥胖组（BMI>30 Kg/m）（11例患者和8例对照）和非肥胖组（BMI<30 Kg/m）（9例患者和7例对照）。
与非肥胖患者相比，肥胖高血压患者摄入葡萄糖加氯化钠后血清AngII显著更高（P = 0.016）。与非肥胖患者相比，肥胖高血压患者摄入葡萄糖加氯化钠后血清钠显著更高（P = 0.009）。与各自的血压正常对照者相比，肥胖患者（葡萄糖后P = 0.03；葡萄糖加氯化钠后P = 0.003）和非肥胖患者（分别为P = 0.000和P = 0.000）的血清醛固酮显著更高。在肥胖和非肥胖患者中，摄入葡萄糖和葡萄糖加氯化钠后血清AngII和醛固酮水平无显著变化，而肥胖患者血清钠显著升高（P = 0.03），非肥胖患者血清钾显著降低（P = 0.001）。
高血压组摄入葡萄糖加氯化钠后AngII和醛固酮分泌未能被抑制或维持不当，这可能是原发性高血压的一种可能机制。
