Injured Podocytes Are Sensitized to Angiotensin II-Induced Calcium Signaling.

ABSTRACT:

Background

Inhibition of angiotensin II (AngII) signaling, a therapeutic mainstay of glomerular kidney diseases, is thought to act primarily through regulating glomerular blood flow and reducing filtration pressure. Although extravascular actions of AngII have been suggested, a direct effect of AngII on podocytes has not been demonstrated in vivo.

Methods

To study the effects of AngII on podocyte calcium levels in vivo, we used intravital microscopy of the kidney in mice expressing the calcium indicator protein GCaMP3.

Results

In healthy animals, podocytes displayed limited responsiveness to AngII stimulation. In contrast, in animals subjected to either adriamycin-induced acute chemical injury or genetic deletion of the podocin-encoding gene Nphs2

SUBMITTER: Binz-Lotter J 

PROVIDER: S-EPMC7062224 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature