Subfornical organ differentially modulates baroreflex function in normotensive and two-kidney, one-clip hypertensive rats
Subfornical organ differentially modulates baroreflex function in normotensive and two-kidney, one-clip hypertensive rats
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DOI：
10.1152/ajpregu.00157.2008
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发表时间：
2008-09-01
影响因子：
2.8
通讯作者：
Rossi, Noreen F.
中科院分区：
文献类型：
--
作者：
Maliszewska-Scislo, Maria;Chen, Haiping;Rossi, Noreen F.
在肾素-血管紧张素系统激活过程中，后脑室周器官如最后区参与调节动脉压力感受性反射。本研究旨在验证穹窿下器（SFO）也可能调节压力感受性反射的假说。本实验以二肾一夹（2K，1C）高血压大鼠为模型，研究内源性激活的肾素-血管紧张素系统。在清醒的假夹和5周的2K，1C大鼠与假或电解损伤的SFO斜坡输注苯肾上腺素和硝普钠期间，确定压力反射功能。损伤显著降低2K，1C大鼠的平均动脉压从158 +/- 7至131 +/- 4 mmHg，但在假夹大鼠中没有。与SFO消融的假夹大鼠相比，SFO损伤的假夹大鼠的肾交感神经活性-平均动脉压关系的上平台和范围显著更高。相反，在2K，1C大鼠中，损毁SFO显著降低肾交感神经活动的压力反射控制的上平台和范围，但仅心率的压力反射反应范围降低。因此，在卸载的压力感受器，SFO差异调节压力反射反应在假夹与2K，1C大鼠。由于SFO损伤不影响血浆血管紧张素II（ANG II），因此SFO损伤的影响不是由ANG II循环水平的变化引起的。这些研究结果支持了一个关键的作用，SFO在肾血管性高血压和压力反射调节交感神经活动在正常和高血压状态下观察到的交感神经兴奋。
During activation of the renin-angiotensin system, hindbrain circumventricular organs such as the area postrema have been implicated in modulating the arterial baroreflex. This study was undertaken to test the hypothesis that the subfornical organ (SFO), a forebrain circumventricular structure, may also modulate the baroreflex. Studies were performed in rats with two-kidney, one-clip (2K, 1C) hypertension as a model of endogenously activated renin-angiotensin system. Baroreflex function was ascertained during ramp infusions of phenylephrine and nitroprusside in conscious sham-clipped and 5-wk 2K, 1C rats with either a sham or electrolytically lesioned SFO. Lesioning significantly decreased mean arterial pressure in 2K, 1C rats from 158 +/- 7 to 131 +/- 4 mmHg but not in sham-clipped rats. SFO-lesioned, sham-clipped rats had a significantly higher upper plateau and range of the renal sympathetic nerve activity-mean arterial pressure relationship compared with sham-clipped rats with SFO ablation. In contrast, lesioning the SFO in 2K, 1C rats significantly decreased both the upper plateau and range of the baroreflex control of renal sympathetic nerve activity, but only the range of the baroreflex response of heart rate decreased. Thus, during unloading of the baroreceptors, the SFO differentially modulates the baroreflex responses in sham-clipped vs. 2K, 1C rats. Since lesioning the SFO did not influence plasma angiotensin II (ANG II), the effects of the SFO lesion are not caused by changes in circulating levels of ANG II. These findings support a pivotal role for the SFO in the sympathoexcitation observed in renovascular hypertension and in baroreflex regulation of sympathetic activity in both normal and hypertensive states.