Renal and Lumbar Sympathetic Nerve Activity During Development of Hypertension in Dahl Salt-Sensitive Rats
Renal and Lumbar Sympathetic Nerve Activity During Development of Hypertension in Dahl Salt-Sensitive Rats
复制标题
达尔盐敏感大鼠高血压发展过程中肾和腰交感神经活动
DOI：
10.1161/hypertensionaha.119.12866
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发表时间：
2019
期刊：
影响因子：
8.3
通讯作者：
Kenju Miki
中科院分区：
文献类型：
--
作者：
Misa Yoshimoto;Yuko Onishi;Naoko Mineyama;Shizuka Ikegame;Mikiyasu Shirai;John W Osborn;Kenju Miki
为了研究交感神经活动（SNA）对高血压发展的贡献，设计了实验，在 Dahl 盐敏感（DS）大鼠中，在 8% 盐负荷诱导的高血压发展过程中连续、同时测量肾脏（RSNA）和腰椎 SNA（LSNA）。雄性 DS 和耐盐大鼠配备双极电极来记录 RSNA 和 LSNA，并配备遥测仪来记录动脉压 (AP)。 DS 和 Dahl 耐盐大鼠在盐负荷开始后的前 3 天内 AP 增加约 10 mm Hg。 DS大鼠中AP从盐负荷第4天到第14天继续逐渐增加33±1mmHg，而Dahl耐盐大鼠中AP保持相同。 RSNA 和 LSNA 在最初几天增加 6% 至 8%，此后逐渐下降，表明 RSNA 和 LSNA 的增加均与 DS 大鼠盐负荷诱导的 AP 逐渐增加没有直接关系。停止盐负荷后，DS 和 Dahl 耐盐大鼠的 AP 压力均恢复至盐前负荷水平。停止盐负荷后RSNA显着增加32±3%，而LSNA在DS大鼠中保持不变，这表明盐敏感机制对钠的丢失而不是钠的增加做出反应，并选择性地激活DS大鼠中的RSNA。总之，RSNA 和 LSNA 不太可能是 DS 大鼠中 8% 盐负荷诱导的 AP 逐渐增加的主要触发因素。
To study the contribution of sympathetic nerve activity (SNA) to the development of hypertension, experiments were designed to continuously and simultaneously measure renal (RSNA) and lumbar SNA (LSNA) during the development of hypertension induced by 8% salt loading in Dahl salt-sensitive (DS) rats. Male DS and salt-resistant rats were instrumented with bipolar electrodes to record RSNA and LSNA and a telemeter to record arterial pressure (AP). AP increased during the first 3 days after the onset of salt loading by ≈10 mm Hg in both DS and Dahl salt-resistant rats. AP continued to increase progressively from day 4 to day 14 of salt loading by 33±1 mm Hg in DS rats, while it remained the same in Dahl salt-resistant rats. RSNA and LSNA increased in the initial few days by 6% to 8%, and decreased gradually thereafter, suggesting that increases in neither RSNA nor LSNA are directly linked with the progressive increase in AP induced by salt loading in DS rats. After the cessation of salt loading, AP pressure returned to the presalt loading level in both DS and Dahl salt-resistant rats. RSNA increased significantly by 32±3% after the cessation of salt loading, while LSNA remained the same in DS rats, suggesting that salt-sensitive mechanisms respond to a loss of sodium, not a gain, and selectively activate RSNA in DS rats. In summary, RSNA and LSNA are not likely to be a primary trigger to initiate the progressive increase in AP induced by 8% salt loading in DS rats.