Disruption of the with no lysine kinase-STE20-proline alanine-rich kinase pathway reduces the hypertension induced by angiotensin II.

ABSTRACT:

Objective

The hypertensive effect of angiotensin II (AngII), a peptide hormone, is dependent on its intrarenal actions and the activation of the renal Na-Cl cotransporter (NCC), by AngII requires integrity of the with no lysine kinase/STE20-proline alanine-rich kinase (WNK/SPAK) signaling pathway. Here, we analyzed if the integrity of the WNK/SPAK pathway is required for AngII infusion to induce arterial hypertension.

Methods

We tested the effect of AngII or aldosterone administration on the blood pressure and on pNCC/NCC ratio in SPAK knock-in mice in which the kinase and thus NCC cannot be activated by WNK kinases. AngII or aldosterone was infused at 1440 or 700 μg/kg per day, respectively, for 14 days using osmotic minipumps. The aldosterone-treated mice were exposed to N

SUBMITTER: Cervantes-Perez LG 

PROVIDER: S-EPMC5757652 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature