高血压患者胰岛素抵抗与内皮细胞功能障碍的关系

Relationship between insulin resistance and endothelial cell dysfunction in essential hypertension patients

目的研究高血压患者胰岛素抵抗(IR)与内皮细胞功能的关系。方法72例原发性高血压(EH)患者分为胰岛素抵抗组(EH-IR)37例和非胰岛素抵抗组(EH非IR)35例,健康对照组25例。用化学法测定各组外周血的一氧化氮(NO)、一氧化氮合酶(NOS)、诱导型一氧化氮合酶(iNOS)和结构型一氧化氮合酶(cNOS)水平。结果EH非IR组和EH-IR组NO水平分别为(64.79±41.96)μmol/L和(74.69±45.66)μmol/L,较健康对照组(110.21±55.79)μmol/L)降低,差异有统计学意义(均P<0.05);EH非IR组和EH-IR组NOS水平分别为(34.74±4.12)kU/L和(33.44±5.09)kU/L,较健康对照组(42.54±4.04)kU/L降低,差异有统计学意义(均P<0.01);iNOS水平分别为(13.86±3.60)kU/L和(13.67±3.95)kU/L,较健康对照组(17.02±2.78)kU/L降低,差异有统计学意义(均P<0.01)。cNOS水平分别为(20.88±3.29)kU/L和(19.77±4.11)kU/L,较健康对照组(25.51±3.51)kU/L降低,差异有统计学意义(均P<0.01)。EH非IR组和EH-IR组NO、NOS、cNOS和iNOS含量的差异无统计学意义(P>0.05)。EH非IR组和EH-IR组的NO,NOS及其亚型水平与IR的相关性均无统计学意义(P>0.05)。结论高血压时内皮细胞释放NO能力的减弱与cNOS表达减弱和iNOS的表达缺陷均有关;高血压患者的IR与内皮系统损伤无明显关联。

Objective To investigate the relationship between insulin resistance and endothelium function in essential hypertension patients. Methods Nitric oxide （NO）, nitric oxide synthase （NOS）, inducible nitric oxide synthase（iNOS） and configurable nitric oxide synthase（cNOS） were detected by chemical colorimetry from the sera of 25 healthy control group and 72 essential hypertension patients, which were divided in two groups： 37 in insulin resistance （EH-IR） group and 35 in non-insulin resistance （EHNIR） group. Results The level of serum NO in EHNIR group and EH-IR group was （64.79± 41.96） μmol/L and （74.69 ± 45.66） μmol/L, both were remarkably lower than that of healthy control group （ P 〈0. 05）. The level of serum NOS in EHNIR group and EH-IR group was （34.74±4.12） kU/L and （33.44±5.09） kU/L,whieh were both significantly lower than that of healthy control group （both P 〈0.01）. iNOS level in EHNIR group and EH-IR group was （13.86±3.60） kU/L and （13.67±3.95） kU/L respectively,both were significantly lower than that of healthy control group （both P 〈0.01）. eNOS level in EHNIR group and EH-IR group was （20.88±3.29） kU/L and （19.77±4.11） kU/L,whieh were both significantly lower than that of healthy control group （both P〈0.01）. There was no significant difference of NO, NOS, iNOS and eNOS between EH-IR group and EHNIR group （all P 〉0. 05）. In neither EH-IR group nor EHNIR group, there was no significant relationship between IR and NO, NOS, iNOS and eNOS respectively. Conclusion The reason why EH patients＇ endothelial cell releases remarkably less NO than healthy control group may be due to their lower expression of eNOS and deficiency of iNOS. There seems no obvious relationship between insulin resistance and endothelial cell dysfunction in EH patients.