Open AccessShort‐term nonpressor angiotensin II infusion stimulates sodium transporters in proximal tubule and distal nephron
Author(s) -
Nguyen Mien T. X.,
Han Jiyang,
Ralph Donna L.,
Veiras Luciana C.,
McDonough Alicia A.
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12496
Subject(s) - endocrinology , medicine , loop of henle , cotransporter , distal convoluted tubule , angiotensin ii , chemistry , nephron , symporter , natriuresis , renin–angiotensin system , renal cortex , sodium , excretion , kidney , blood pressure , transporter , biology , biochemistry , organic chemistry , gene
In Sprague Dawley rats, 2‐week angiotensin II (Ang II ) 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 Ang II 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 Ang II (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 Ang II and vehicle infused rats. The 3‐day nonpressor Ang II infusion significantly increased the abundance of PT Na + /H + exchanger 3 ( NHE 3), cortical TALH Na‐K‐2Cl cotransporter 2 ( NKCC 2), distal convoluted tubule ( DCT ) Na‐Cl cotransporter ( NCC ), and cortical CD EN aC subunits. Additionally, phosphorylation of cortical NKCC 2, NCC , and STE 20/ SPS 1‐related proline–alanine‐rich kinase ( SPAK ) were increased; medullary NKCC 2 and SPAK were not altered. In conclusion, 3‐day Ang II infusion provokes PT NHE 3 accumulation as well as NKCC 2, NCC , and SPAK accumulation and activation in a prehypertensive phase before evidence for intrarenal angiotensinogen accumulation.