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Crosstalk between the renal sympathetic nerve and intrarenal angiotensin II modulates proximal tubular sodium reabsorption
Author(s) -
Pontes Roberto B.,
Girardi Adriana C. C.,
Nishi Erika E.,
Campos Ruy R.,
Bergamaschi Cássia T.
Publication year - 2015
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep085075
Subject(s) - renal sodium reabsorption , reabsorption , crosstalk , endocrinology , medicine , angiotensin ii , renin–angiotensin system , renal physiology , chemistry , sodium , kidney , receptor , physics , blood pressure , organic chemistry , optics
New FindingsWhat 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.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.