Department of Biological Sciences, Institute of Exact and Biological Sciences and NUPEB, Federal University of Ouro Preto, Ouro Preto, (MG), Brazil.
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, (SP), Brazil.
Sci Rep. 2017 Jul 18;7(1):5655. doi: 10.1038/s41598-017-05984-9.
In this study, we investigated some mechanisms involved in sodium-dependent hypertension of rats exposed to chronic salt (NaCl) intake from weaning until adult age. Weaned male Wistar rats were placed under high (0.90% w/w, HS) or regular (0.27% w/w, Cont) sodium diets for 12 weeks. Water consumption, urine output and sodium excretion were higher in HS rats compared to control. Blood pressure (BP) was directly measured by the arterial catheter and found 13.8% higher in HS vs Cont rats. Ganglionic blockade with hexamethonium caused greater fall in the BP of HS rats (33%), and central antagonism of AT receptors (losartan) microinjected into the lateral ventricle reduced BP level of HS, but not of Cont group. Heart rate variability analysis revealed sympathetic prevalence on modulation of the systolic interval. HS diet did not affect creatinine clearance. Kidney histological analysis revealed no significant change in renal corpuscle structure. Sodium and potassium concentrations in CSF were found higher in HS rats despite no change in plasma concentration of these ions. Taken together, data suggest that animals exposed to chronic salt intake to a level close to that reported for human' diet since weaning lead to hypertension, which appears to rely on sodium-driven neurogenic mechanisms.
在这项研究中，我们研究了一些与从断奶到成年期持续摄入盐（NaCl）有关的钠依赖性高血压大鼠的机制。雄性 Wistar 大鼠断奶后接受高钠（0.90%w/w，HS）或正常钠（0.27%w/w，Cont）饮食 12 周。与对照组相比，HS 组大鼠的水摄入量、尿量和钠排泄量更高。通过动脉导管直接测量血压，发现 HS 组大鼠的血压比 Cont 组高 13.8%。HS 大鼠的交感神经节阻断剂六烃季铵（hexamethonium）引起的血压下降幅度更大（33%），而向侧脑室注射的 AT 受体中枢拮抗剂（losartan）降低了 HS 大鼠的血压水平，但对 Cont 组没有影响。心率变异性分析显示，交感神经对收缩期间隔的调节占主导地位。HS 饮食对肌酐清除率没有影响。肾脏组织学分析显示，尽管 CSF 中钠离子和钾离子的浓度没有变化，但 HS 大鼠的肾小体结构没有明显变化。
总而言之，这些数据表明，从断奶到成年期持续摄入接近人类饮食水平的盐会导致动物高血压，这种高血压似乎依赖于钠驱动的神经源性机制。
