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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Renal nerve stimulation leads to the activation of the Na+/H+ exchanger isoform 3 via angiotensin II type I receptor

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Author(s):
Pontes, Roberto B. [1] ; Crajoinas, Renato O. [2] ; Nishi, Erika E. [1] ; Oliveira-Sales, Elizabeth B. [1] ; Girardi, Adriana C. [2] ; Campos, Ruy R. [1] ; Bergamaschi, Cassia T. [1]
Total Authors: 7
Affiliation:
[1] Univ Fed Sao Paulo, Dept Fisiol, Disciplina Fisiol Cardiovasc, BR-04023060 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Sch Med, Heart Inst InCor, Lab Genet & Mol Cardiol, Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY; v. 308, n. 8, p. F848-F856, APR 15 2015.
Web of Science Citations: 20
Abstract

Renal nerve stimulation at a low frequency (below 2 Hz) causes water and sodium reabsorption via alpha(1)-adrenoreceptor tubular activation, a process independent of changes in systemic blood pressure, renal blood flow, or glomerular filtration rate. However, the underlying mechanism of the reabsorption of sodium is not fully understood. Since the sympathetic nervous system and intrarenal ANG II appear to act synergistically to mediate the process of sodium reabsorption, we hypothesized that low-frequency acute electrical stimulation of the renal nerve (ESRN) activates NHE3-mediated sodium reabsorption via ANG II AT(1) receptor activation in Wistar rats. We found that ESRN significantly increased urinary angiotensinogen excretion and renal cortical ANG II content, but not the circulating angiotensinogen levels, and also decreased urinary flow and pH and sodium excretion via mechanisms independent of alterations in creatinine clearance. Urinary cAMP excretion was reduced, as was renal cortical PKA activity. ESRN significantly increased NHE3 activity and abundance in the apical microvillar domain of the proximal tubule, decreased the ratio of phosphorylated NHE3 at serine 552/total NHE3, but did not alter total cortical NHE3 abundance. All responses mediated by ESRN were completely abolished by a losartan-mediated AT(1) receptor blockade. Taken together, our results demonstrate that higher NHE3-mediated proximal tubular sodium reabsorption induced by ESRN occurs via intrarenal renin angiotensin system activation and triggering of the AT(1) receptor/inhibitory G-protein signaling pathway, which leads to inhibition of cAMP formation and reduction of PKA activity. (AU)

FAPESP's process: 13/22522-9 - Role of renal sympathetic nerves on cardiovascular and renal alterations in renovascular hypertension
Grantee:Ruy Ribeiro de Campos Junior
Support Opportunities: Regular Research Grants
FAPESP's process: 12/10146-0 - Molecular mechanisms of regulation of the proximal tubular function in hypertension
Grantee:Adriana Castello Costa Girardi
Support Opportunities: Regular Research Grants