DiBona G F
Departments of Internal Medicine and Physiology, University of Iowa College of Medicine, and Veterans Administration Medical Center, Iowa City, Iowa, USA.
Hypertension. 2000 Dec;36(6):1083-8. doi: 10.1161/01.hyp.36.6.1083.
Increases in renal sympathetic nerve activity regulate the functions of the nephron, the vasculature, and the renin-containing juxtaglomerular granular cells. Because increased activity of the renin-angiotensin system can also influence nephron and vascular function, it is important to understand the interactions between the renal sympathetic nerves and the renin-angiotensin system in the control of renal function. These interactions can be intrarenal, for example, the direct (by specific innervation) and indirect (by angiotensin II) contributions of increased renal sympathetic nerve activity to the regulation of renal function. The effects of increased renal sympathetic nerve activity on renal function are attenuated when the activity of the renin-angiotensin system is suppressed or antagonized with ACE inhibitors or angiotensin II-type AT(1)-receptor antagonists. The effects of intrarenal administration of angiotensin II are attenuated after renal denervation. These interactions can also be extrarenal, for example, in the central nervous system, wherein renal sympathetic nerve activity and its arterial baroreflex control are modulated by changes in activity of the renin-angiotensin system. In addition to the circumventricular organs, whose permeable blood-brain barrier permits interactions with circulating angiotensin II, there are interactions at sites behind the blood-brain barrier that depend on the influence of local angiotensin II. The responses to central administration of angiotensin II-type AT(1)-receptor antagonists into the ventricular system or microinjected into the rostral ventrolateral medulla are modulated by changes in activity of the renin-angiotensin system produced by physiological changes in dietary sodium intake. Similar modulation is observed in pathophysiological models wherein activity of both the renin-angiotensin and sympathetic nervous systems is increased (eg, congestive heart failure). Thus, both renal and extrarenal sites of interaction between the renin-angiotensin system and renal sympathetic nerve activity are involved in influencing the neural control of renal function.
肾交感神经活动增强可调节肾单位、血管系统以及含肾素的球旁颗粒细胞的功能。由于肾素 - 血管紧张素系统活性增强也会影响肾单位和血管功能,因此了解肾交感神经与肾素 - 血管紧张素系统在肾功能控制中的相互作用至关重要。这些相互作用可发生在肾内,例如,肾交感神经活动增强对肾功能调节的直接(通过特定神经支配)和间接(通过血管紧张素II)作用。当肾素 - 血管紧张素系统的活性被ACE抑制剂或血管紧张素II 1型(AT1)受体拮抗剂抑制或拮抗时,肾交感神经活动增强对肾功能的影响会减弱。肾去神经支配后,肾内给予血管紧张素II的作用会减弱。这些相互作用也可发生在肾外,例如在中枢神经系统中,肾交感神经活动及其动脉压力反射控制会受到肾素 - 血管紧张素系统活性变化的调节。除了室周器官,其可渗透的血脑屏障允许与循环中的血管紧张素II相互作用外,在血脑屏障后的部位也存在相互作用,这取决于局部血管紧张素II的影响。向脑室系统或微量注射到延髓头端腹外侧的血管紧张素II 1型(AT1)受体拮抗剂的中枢给药反应,会受到饮食钠摄入量生理变化所产生的肾素 - 血管紧张素系统活性变化的调节。在肾素 - 血管紧张素和交感神经系统活性均增加的病理生理模型(如充血性心力衰竭)中也观察到类似的调节。因此,肾素 - 血管紧张素系统与肾交感神经活动之间的肾内和肾外相互作用部位均参与影响肾功能的神经控制。