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

Abstract

New Findings r 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 (AT 1 ) receptor by angiotensin II. r 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 AT 1 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 (AT 1 ) 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 AT 1 receptor, triggered an intracellular pathway activating NHE3 in the renal cortex, leading to antinatriuresis and antidiuresis. Pharmacological blockade of the AT 1 receptor with losartan prior to RNS abolished both the functional and the molecular responses, suggesting that intrarenal Ang II acting via the AT 1 receptor is a major factor for NHE3-mediated sodium and water reabsorption induced by RNS.

Is our current understanding and management of nocturia allowing improved care? International Consultation on Incontinence‐Research Society 2018

“…These data suggest an association between an increased sympathetic tone and NP, however in men the presence of the prostate confounds this association. Similarly, Pontes et al showed how sympathetic overactivity increases renal sodium reabsorption by activation of renin‐angiotensin and Na/H exchanger. More research is needed in this field to reach definitive conclusions.…”

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

“…NHE3 plays a pivotal role in salt and fluid reabsorption in the proximal tubule, and is required for ANG II-induced hypertension in mice (580). It should also be noted that renal sympathetic nerve stimulation leads to NHE3-dependent proximal tubule sodium reabsorption via enhanced generation of intrarenal ANG II (831,832). ANG II activates NHE3 via Ca 2ϩ , calmodulin (CaM), and CaMKII.…”

Immunohistochemical expression of intrarenal renin angiotensin system components in response to tempol in rats fed a high salt diet

“…Moreover, these results suggest, that intrarenal mechanisms that regulate the differential expression of Ang II and ACE2 exacerbated by a high-sodium diet, would not be a dependent mechanism of oxidative stress. In this sense it has been shown that in physiological conditions, acute renal sympathetic nerve activity modulates sodium reabsorption by increasing intrarenal Ang II generation and activation of the luminal membrane AT1R[44]. It has been recently shown that activation of renal nervous system results in higher levels of intrarenal angiotensinogen and Ang II independent of changes in renal function and systemic RAS[45].…”