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背景长期高盐摄入可导致高血压,但导致其血压升高的机制目前仍未明确,对是否因为钠水潴留,还是由于交感神经肾上腺系统(SAS)或肾素血管紧张素系统(RAS)的兴奋导致血压升高,目前仍存许多争议。目的探讨不同钠和水的摄入对大鼠血压的影响。方法将20只Wistar大鼠根据每天的不同钠、水摄入随机分成4组:低盐自由饮水组(n=5);低盐控制摄水组(n=5),即每天仅给予生理需要量摄水40mL;高盐自由饮水组(n=5);高盐控制摄水组(n=5),即每天仅给予生理需要量摄水40mL。每天测量各组的摄水量,使用代谢笼收集尿量,计算摄水量和尿量差值;每周测量体质量和鼠尾动脉收缩压1次,共8周。8周后采血标本,免疫酶联法测定血去甲肾上腺素(NE)和血管紧张素Ⅱ(AngⅡ)。结果高盐各组血压明显升高,体质量增长缓慢、摄水-尿量差也明显减少,同时血NE升高而AngⅡ下降,与低盐各组比较差异存在统计学意义(P<0.01);而高盐控水组与高盐自由饮水组8周后比较,血压下降[(156.2±2.3)比(166.7±2.2)mmHg]、NE升高[(3.5±0.6)比(2.2±0.5)μg/L],AngⅡ下降[(203.5±98.0)比(233.4±101.7)ng/L](均P<0.01)。结论高盐摄入会导致血压升高,但这种血压升高可能与钠水潴留、RAS过度激活无关,起主导作用的可能是交感神经的过度激活。
Background Long-term high salt intake can lead to high blood pressure, but the mechanism leading to its elevated blood pressure is still unclear. Whether it is due to sodium-water retention or due to sympathetic adrenal system (SAS) or renin-angiotensin system (RAS) The excitement led to high blood pressure, there are still many controversies. Objective To investigate the effects of different sodium and water intake on blood pressure in rats. Methods Twenty Wistar rats were randomly divided into four groups according to daily intake of sodium and water: low salinity free water (n = 5); low salinity control water intake (n = 5) The amount of water intake 40mL; high salt free drinking water group (n = 5); high salt control water intake group (n = 5), that is, giving only physical requirements daily water intake 40mL. The water intake of each group was measured daily, the urine volume was collected using metabolic cage, and the difference between water intake and urine output was calculated. Body mass and systolic pressure of rat tail artery were measured once a week for 8 weeks. Blood samples were taken after 8 weeks and the levels of NE and Ang Ⅱ were measured by enzyme-linked immunosorbent assay. Results Compared with the low salt group, the blood pressure increased significantly, the body weight increased slowly, the difference of water intake and urine volume decreased significantly, while the blood NE increased and AngⅡ decreased, there was statistical significance (P <0.01) (156.2 ± 2.3) vs (166.7 ± 2.2) mmHg] and NE elevation [(3.5 ± 0.6) vs (2.2 ± 0.5), respectively] μg / L], AngⅡdecreased [(203.5 ± 98.0) vs (233.4 ± 101.7) ng / L] (all P <0.01). Conclusions High salt intake may lead to an increase in blood pressure. However, this increase in blood pressure may be related to sodium and water retention and RAS overactivity. The predominant effect may be the over-activation of sympathetic nerve.