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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Physiol+Rep
2015 ; 3
(9
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Short-term nonpressor angiotensin II infusion stimulates sodium transporters in
proximal tubule and distal nephron
#MMPMID26347505
Nguyen MT
; Han J
; Ralph DL
; Veiras LC
; McDonough AA
Physiol Rep
2015[Sep]; 3
(9
): ä PMID26347505
show ga
In Sprague Dawley rats, 2-week angiotensin II (AngII) infusion increases Na(+)
transporter abundance and activation from cortical thick ascending loop of Henle
(TALH) to medullary collecting duct (CD) and raises blood pressure associated
with a pressure natriuresis, accompanied by depressed Na(+) transporter abundance
and activation from proximal tubule (PT) through medullary TALH. This study tests
the hypothesis that early during AngII infusion, before blood pressure raises,
Na(+) transporters' abundance and activation increase all along the nephron. Male
Sprague Dawley rats were infused via osmotic minipumps with a subpressor dose of
AngII (200 ng/kg/min) or vehicle for 3 days. Overnight urine was collected in
metabolic cages and sodium transporters' abundance and phosphorylation were
determined by immunoblotting homogenates of renal cortex and medulla. There were
no significant differences in body weight gain, overnight urine volume, urinary
Na(+) and K(+) excretion, or rate of excretion of a saline challenge between
AngII and vehicle infused rats. The 3-day nonpressor AngII infusion significantly
increased the abundance of PT Na(+)/H(+) exchanger 3 (NHE3), cortical TALH
Na-K-2Cl cotransporter 2 (NKCC2), distal convoluted tubule (DCT) Na-Cl
cotransporter (NCC), and cortical CD ENaC subunits. Additionally, phosphorylation
of cortical NKCC2, NCC, and STE20/SPS1-related proline-alanine-rich kinase (SPAK)
were increased; medullary NKCC2 and SPAK were not altered. In conclusion, 3-day
AngII infusion provokes PT NHE3 accumulation as well as NKCC2, NCC, and SPAK
accumulation and activation in a prehypertensive phase before evidence for
intrarenal angiotensinogen accumulation.