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首页> 外文期刊>American Journal of Physiology >Effect of endogenous angiotensin II on the frequency response of the renal vasculature.
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Effect of endogenous angiotensin II on the frequency response of the renal vasculature.

机译：内源性血管紧张素II对肾血管频率响应的影响。

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摘要

The renal vasculature functions as an efficient low-pass filter of the multiple frequencies contained within renal sympathetic nerve activity. This study examined the effect of angiotensin II on the frequency response of the renal vasculature. Physiological changes in the activity of the endogenous renin-angiotensin system were produced by alterations in dietary sodium intake. The frequency response of the renal vasculature was evaluated using pseudorandom binary sequence renal nerve stimulation, and the role of angiotensin II was evaluated by the administration of the angiotensin II AT(1)-receptor antagonist losartan. In low-sodium-diet rats with increased renin-angiotensin system activity, losartan steepened the renal vascular frequency response (i.e., greater attenuation); this was not seen in normal- or high-sodium-diet rats with normal or decreased renin-angiotensin system activity. Analysis of the transfer function from arterial pressure to renal blood flow, i.e., dynamic autoregulation, showed that the tubuloglomerular feedback but not the myogenic component was enhanced in low- and normal- but not in high-sodium-diet rats and that this was reversed by losartan administration. Thus physiological increases in endogenous renin-angiotensin activity inhibit the renal vascular frequency response to renal nerve stimulation while selectively enhancing the tubuloglomerular feedback component of dynamic autoregulation of renal blood flow.
机译：肾脉管系统可作为肾交感神经活动中所含多个频率的有效低通滤波器。这项研究检查了血管紧张素II对肾血管频率响应的影响。内源性肾素-血管紧张素系统活性的生理变化是通过饮食中钠摄入量的变化而产生的。使用伪随机二进制序列肾神经刺激评估肾血管的频率响应，并通过施用血管紧张素II AT（1）-受体拮抗剂洛沙坦评估血管紧张素II的作用。在肾素-血管紧张素系统活性增加的低钠饮食大鼠中，氯沙坦使肾血管频率反应变陡（即更大的衰减）。这在肾素-血管紧张素系统活性正常或降低的正常或高钠饮食的大鼠中未观察到。从动脉压到肾血流量的传递函数的分析，即动态自动调节，表明低钠和正常钠饮食大鼠的肾小管肾小球反馈增强，但肌原性成分没有增强，而高钠饮食的大鼠则没有由氯沙坦管理。因此，内源性肾素-血管紧张素活性的生理增加抑制了对肾神经刺激的肾血管频率响应，同时选择性地增强了肾血流动态自动调节的肾小管肾小球反馈成分。

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