肥胖高血压患者血清瘦素与肾素-血管紧张素-醛固酮系统的相关性研究

Study on the relationship between serum leptin and relationship between serum leptin and renin-angiotensin-aldosterone system in obese hypertensive patients

目的分析肥胖高血压患者瘦素与肾素-血管紧张素-醛固酮系统(RAAS)的相关性,并探讨服用盐酸贝那普利8周后RAAS活性变化与瘦素水平变化之间的关系。方法入选单纯肥胖患者、肥胖高血压Ⅰ级患者、肥胖高血压Ⅱ级患者、健康对照者各50例,每组男性、女性各25例。收集一般资料,包括年龄、体质指数、腰围、腰臀比和血压。检测血清瘦素、肾素(PRA)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)水平,分析各组血清瘦素水平与RAAS活性的相关性,以及全部肥胖患者的血压水平与瘦素水平、RAAS活性的相关性。同时观察应用血管紧张素转换酶抑制剂盐酸贝那普利治疗8周后,肥胖高血压患者的血清瘦素、PRA、AngⅡ和ALD水平的变化。结果肥胖高血压患者的血清瘦素、PRA、AngⅡ和ALD水平均明显高于单纯肥胖组和健康对照组,且与高血压分级有关,差异均有统计学意义(P<0.05或P<0.01)。肥胖高血压患者的血清瘦素水平与PRA、AngⅡ和ALD水平呈正相关(r=0.497、0.861、0.628,P<0.05或P<0.01)。单纯肥胖组的血清瘦素水平与ALD水平呈正相关(r=0.675,P<0.01)。全部肥胖患者的血压水平与血清瘦素、PRA、AngⅡ和ALD水平呈正相关(r=0.519、0.629、0.875、0.539,P<0.05或P<0.01)。应用盐酸贝那普利治疗后,肥胖高血压患者的血清瘦素、AngⅡ和ALD水平明显降低(均为P<0.01)。结论肥胖人群存在瘦素抵抗,瘦素可能通过影响RAAS活性导致肥胖者血压升高。

Objective To analyze the relationship between serum leptin and RAAS in obese hypertensive patients, and to investigate the relationship between RAAS activity and leptin level after 8 weeks of taking benazepril hydrochloride. Methods A total of 150 patients with obesity（ n = 50）or obesity with hypertension grade 1 （ n = 50） or grade 2 （ n = 50）, and 50 healthy controls were enrolled. Data including age, body mass index, waist circumference, waist-hip ratio and blood pressure were collected and the levels of serum leptin, PRA, Ang Ⅱ, ALD were measured for all subjects, and the correlation between serum leptin level and RAAS activity were analyzed. Meanwhile, the correlation between blood pressure level and leptin level, RAAS activity in all obesity patients were analyzed. The changes of serum leptin, PRA, Ang Ⅱ , ALD level were investigated in obesity patients with hypertension after 8 weeks treatment with benazepril hydrochloride. Results The levels of serum leptin, PRA, Ang Ⅱ and ALD in obesity patients with hypertension were significantly higher than those in simple obesity patients and healthy controls, and were related to hypertension grading, the differences were statistically significant （ P 〈 0. 05 or P 〈 0. 01 ）. A positive correlation was found between serum leptin level and PRA, Ang Ⅱ , ALD in obesity patients with hypertension（ r = 0. 497,0. 861,0. 628 ,P 〈 0. 05 or P 〈 0. 01 ）. And a positive correlation was found between serum leptin and ALD in obesity patients（ r = 0. 675, P 〈 0. 01 ）. A positive eorrelation was found between blood pressure level and serum leptin, PRA, Ang Ⅱ , ALD level in all obesity patients （r = 0. 519,0. 629, 0. 875,0. 539 ,P 〈 0. 05 or P 〈 0. 01 ） . The levels of serum leptin, Ang Ⅱ and ALD were significantly decreased after treatment with benazepril hydrochloride in obesity patients with hypertension（ all P 〈 0. 01 ）. Conclusions Leptin resistance exists in obese people. Leptin could lead to an increase of blood pressure in obesity patients with hypertension through regulating the RAAS activity.