Premium
Electrical stimulation of the renal sympathetic nerve increases NHE3‐mediated sodium reabsorption via angiotensin II AT1 receptor (892.29)
Author(s) -
Pontes Roberto,
Crajoinas Renato,
Veiga Gláucia,
Girardi Adriana,
Campos Ruy,
Bergamaschi Cássia
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.892.29
Subject(s) - renal sodium reabsorption , losartan , endocrinology , medicine , reabsorption , stimulation , angiotensin ii , angiotensin ii receptor type 1 , renin–angiotensin system , chemistry , kidney , sodium , natriuresis , receptor , blood pressure , organic chemistry
The role of renal sympathetic nerve activity on sodium and water handling by the kidneys has not been fully investigated. This study aimed to evaluate the effect of acute sympathetic renal nerve electrical stimulation (RNES) on proximal tubule NHE3 regulation and the possible role of Ang II in mediating this effect. To this end, male Wistar rats (250g‐300g) were uninephrectomized and one week later were divided in three independent groups: sham (renal sympathetic nerve activity registered for 1h); RNES for 1h, (15V, 1.5Hz and 0.5 ms) and RNES treated with Losartan (10 mg/kg, i.v.). Electrical stimulation produced reduction in the levels of NHE3 phosphorylation at the residue serine 552 (100±5% vs. 66±3%), increased activity of renal cortical PKA, and a reduction in urinary output (0.0235±0.006 vs 0.007±0.002 uL/min/Kg) and urinary sodium excretion (1.48±0.2 vs. 0.58±0.1 uEq/min/kg). These anti‐natriuretic effects were completely prevented by injection of Losartan. Taken together, our findings suggest that RNES increases NHE3‐mediated sodium reabsorption and that these effects are mostly, if not all, dependent on Ang II.