盐敏感性高血压病患者静脉盐水负荷后血管紧张素Ⅱ的受抑状态与心钠素及钠代谢

Suppression of angiotensin II after acute saline loading associates with changes of plasma atrial natriuretic peptide and sodium metabolism in patients salt-sensitive hypertension

目的 探讨盐敏感性高血压病患者盐负荷前、后肾素 血管紧张素系统及心钠素 (ANP)变化规律及与钠代谢关系。方法 对 173例 1、2级高血压病患者进行急性静脉盐水负荷试验筛选盐敏感者 ,测定盐负荷前、后血浆血管紧张素Ⅱ (AngⅡ )、ANP ,尿钠排泄量及红细胞钠含量。结果 盐敏感性高血压病患者盐水负荷后AngⅡ受抑不足 ,血浆ANP代偿性分泌减少 ,尿钠排泄延缓 ,红细胞钠含量增加 ;盐敏感性高血压病患者盐水负荷后AngⅡ未受抑者血浆ANP降低 ,尿钠排泄量显著低于AngⅡ受抑者 ,红细胞钠含量显著增加。结论 盐敏感性高血压盐负荷后肾素 血管紧张素系统改变呈非匀一性 ,AngⅡ未受抑者有明显的钠代谢障碍 ;盐负荷后盐敏感性高血压病患者有内源性ANP分泌不足表现。

Objective To explore the changes of plasma angiotensin Ⅱ( AngⅡ), atrial natriuretic peptide(ANP) after sodium loading patients and the relation to urinary natrium excretion in patients with salt-sensitive hypertension. Methods Salt-sensitive were screened in 173 class 1 and class 2 essential hypertensives.Plasma Ang Ⅱand ANP were determined using radioimmunoassay. Results Ang Ⅱ was not adequately suppressed, plasma ANP compensatory secretion decreased urinary Na + excretion was delayed, Na + in RBC was increased after acute salt loading patients. The plasma ANP level was lower, and 24h urinary Na + secretion was also lower in patients with AngⅡ unsuppressed state than those with AngⅡ suppressed salt after salt loading. Conclusion The changes of renin-angiotensin-system is not homogeneous after salt loading. Severe sodium metabolism abnormalities were observed in patients with AngⅡ unsuppessed state and the endogenous ANP secretion was impaired in salt-sensitive hypertensives.