Central Angiotensin II type 1 receptor deficiency alleviates renal fibrosis by reducing sympathetic nerve discharge in nephrotoxic folic acid-induced chronic kidney disease.

ABSTRACT:

Background

Fibrosis after nephrotoxic injury is common. Activation of the paraventricular nucleus (PVN) renin-angiotensin system (RAS) and sympathetic nervous system (SNS) are common mechanism of renal fibrosis. However, there have limited knowledge about which brain regions are most affected by Angiotensin II (Ang II) after nephrotoxic injury, what role does Angiotensin II type 1a receptors (AT1R) signaling play and how this affects the outcomes of the kidneys.

Methods

In nephrotoxic folic acid-induced chronic kidney disease (FA-CKD) mouse models, we have integrated retrograde tracer techniques with studies on AT1afl/fl mice to pinpoint an excessively active central pathway that connects the paraventricular nucleus (PVN) to the rostral ventrolateral medulla (RVLM). This pat

SUBMITTER: Wan Q 

PROVIDER: S-EPMC11439387 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature