Crosstalk between the renal sympathetic nerve and intrarenal angiotensin II modulates proximal tubular sodium reabsorption

• Published in: Experimental physiology 2015-05, Vol.100 (5), p.502-506
• Main Authors: Pontes, Roberto B., Girardi, Adriana C. C., Nishi, Erika E., Campos, Ruy R., Bergamaschi, Cássia T.
• Format: Article
• Language: English
• Subjects: Angiotensin II - metabolism; Animals; Glomerular Filtration Rate - physiology; Humans; Kidney - blood supply; Kidney - metabolism; Renin-Angiotensin System - physiology; Sodium - metabolism; Sympathetic Nervous System - physiology
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/EP085075

New Findings 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.