Pontes Roberto B, Girardi Adriana C C, Nishi Erika E, Campos Ruy R, Bergamaschi Cássia T
Department of Physiology, Division of Cardiovascular Physiology, Federal University of Sao Paulo, São Paulo, SP, Brazil.
Exp Physiol. 2015 Apr 20;100(5):502-6. doi: 10.1113/EP085075.
What is the topic of this review? The sympathetic control of renal sodium tubular reabsorption is dependent on activation of the intrarenal renin-angiotensin system and activation of the angiotensin II type 1 (AT1 ) receptor by angiotensin II. What advances does it highlight? Despite the fact that the interaction between the sympathetic nervous system and angiotensin II regarding salt reabsorption is a well-known classical mechanism for the maintenance of extracellular volume homeostasis, the underlying molecular signalling is not clearly understood. It has been shown recently that renal nerve stimulation increases intrarenal angiotensin II and activates the AT1 receptor, triggering a signalling cascade that leads to elevations of Na(+) -H(+) exchanger isoform 3-mediated tubular transport. In this short review, the crosstalk between intrarenal angiotensin II and renal nerve activity and its effect on sodium reabsorption is addressed. In this review, we address the importance of the interaction between the sympathetic nervous system and intrarenal renin-angiotensin system in modulating renal tubular handling of sodium and water. We have recently shown that increased Na(+) -H(+) exchanger isoform 3 (NHE3) activity induced by renal nerve stimulation (RNS) depends on the activation of the angiotensin II type 1 (AT1 ) receptor by angiotensin II (Ang II). Low-frequency RNS resulted in higher levels of intrarenal angiotensinogen and Ang II independent of changes in blood pressure, the glomerular filtration rate and systemic angiotensinogen. Angiotensin II, via the AT1 receptor, triggered an intracellular pathway activating NHE3 in the renal cortex, leading to antinatriuresis and antidiuresis. Pharmacological blockade of the AT1 receptor with losartan prior to RNS abolished both the functional and the molecular responses, suggesting that intrarenal Ang II acting via the AT1 receptor is a major factor for NHE3-mediated sodium and water reabsorption induced by RNS.
本综述的主题是什么？肾钠重吸收的交感神经控制依赖于肾内肾素-血管紧张素系统的激活以及血管紧张素II对1型血管紧张素II（AT1）受体的激活。它突出了哪些进展？尽管交感神经系统与血管紧张素II在盐重吸收方面的相互作用是维持细胞外液容量稳态的一种众所周知的经典机制，但其潜在的分子信号传导尚不清楚。最近的研究表明，肾神经刺激会增加肾内血管紧张素II并激活AT1受体，引发信号级联反应，导致由Na(+) -H(+)交换体3介导的肾小管转运增加。在这篇简短的综述中，探讨了肾内血管紧张素II与肾神经活动之间的相互作用及其对钠重吸收的影响。在本综述中，我们阐述了交感神经系统与肾内肾素-血管紧张素系统之间的相互作用在调节肾小管对钠和水的处理中的重要性。我们最近发现，肾神经刺激（RNS）诱导的Na(+) -H(+)交换体3（NHE3）活性增加依赖于血管紧张素II（Ang II）对1型血管紧张素II（AT1）受体的激活。低频RNS导致肾内血管紧张素原和Ang II水平升高，而与血压、肾小球滤过率和全身血管紧张素原的变化无关。血管紧张素II通过AT1受体触发肾皮质中激活NHE3的细胞内途径，导致尿钠排泄减少和抗利尿作用。在RNS之前用氯沙坦对AT1受体进行药理阻断消除了功能和分子反应，这表明通过AT1受体起作用的肾内Ang II是RNS诱导的NHE3介导的钠和水重吸收的主要因素。
