The aim of our study is to investigate the sympathetic output and baroreflex via renal sympathetic nerve activity (RSNA) recording in a model of severe hypertension which exhibits arterial, cardiac, and renal damages, the spontaneously hypertensive rat (SHR) under lowered NO bioavailability. SHR are treated from 18 to 20 weeks of age with a low dose of L-NAME, a NO synthase inhibitor, in drinking water (SHRLN) and compared to SHR and normotensive Wistar Kyoto (WKY) rats. After the two-week treatment, rats are anesthetized for RSNA, mean blood pressure (MBP), and heart rate (HR) recording. MBP is higher in SHR than in WKY and higher in SHRLN than in SHR. Compared to WKY, SHR displays an alteration in the baroreflex with a displacement of the sympathoinhibition curve to highest pressures; this displacement is greater in SHRLN rats. The bradycardic response is reduced in SHRLN compared to both SHR and WKY. In hypertensive rats, SHR and SHRLN, basal RSNA is modified, the maximal amplitude of burst is reduced, but minimal values are increased, indicating an increased basal RSNA with reduced bursting activity. The temporal correlation between RSNA and HR is preserved in SHR but altered in 10 SHRLN out of 10. The RSNA inhibition triggered by the Bezold–Jarisch reflex activation is not modified in hypertensive rats, SHR or SHRLN, in contrast to that triggered by the baroreflex. Histological analysis of the carotid bifurcation does not reveal any abnormality in SHRLN at the level of the carotid sinus. In conclusion, data indicate that the sympathetic outflow is altered in SHRLN with a strong reduction of the baroreflex sympathoinhibition and suggest that its central pathway is not involved. These additional results on SHRLN also confirm the usefulness of this model of severe hypertension with multiple target organ damages.

中文翻译：

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使用与一氧化氮慢性减少相关的自发性高血压大鼠模型，在严重高血压的背景下，交感神经活动和压力反射发生强烈改变

我们研究的目的是通过肾交感神经活动 (RSNA) 记录在严重高血压模型中调查交感神经输出和压力反射，该模型表现出动脉、心脏和肾脏损伤，自发性高血压大鼠 (SHR) 在 NO 生物利用度降低的情况下。SHR 在 18 至 20 周龄时用低剂量的 L-NAME（一种 NO 合酶抑制剂）在饮用水 (SHRLN) 中进行治疗，并与 SHR 和血压正常的 Wistar Kyoto (WKY) 大鼠进行比较。在两周的治疗后，大鼠被麻醉以进行 RSNA、平均血压 (MBP) 和心率 (HR) 记录。SHR 的 MBP 高于 WKY，SHRLN 的 MBP 高于 SHR。与 WKY 相比，SHR 表现出压力反射的改变，交感神经抑制曲线位移到最高压力；这种位移在 SHRLN 大鼠中更大。与 SHR 和 WKY 相比，SHRLN 的心动过缓反应降低。在高血压大鼠 SHR 和 SHRLN 中，基础 RSNA 被修改，爆发的最大振幅降低，但最小值增加，表明基础 RSNA 增加，爆发活动减少。RSNA 和 HR 之间的时间相关性在 SHR 中得以保留，但在 10 个 SHRLN 中的 10 个发生改变。与压力反射触发的抑制相比，由 Bezold-Jarisch 反射激活触发的 RSNA 抑制在高血压大鼠、SHR 或 SHRLN 中未改变. 颈动脉分叉的组织学分析未显示颈动脉窦水平的 SHRLN 有任何异常。综上所述，数据表明 SHRLN 中的交感神经流出发生改变，压力反射交感神经抑制强烈降低，并表明其中枢通路不参与。这些关于 SHRLN 的额外结果也证实了这种具有多个靶器官损伤的严重高血压模型的有用性。