FK506 regulates Ca²⁺ release evoked by inositol 1,4,5-trisphosphate independently of FK-binding protein in endothelial cells.

ABSTRACT:

Background and purpose

FK506 and rapamycin are modulators of FK-binding proteins (FKBP) that are used to suppress immune function after organ and hematopoietic stem cell transplantations. The drugs share the unwanted side-effect of evoking hypertension that is associated with reduced endothelial function and nitric oxide production. The underlying mechanisms are not understood. FKBP may regulate IP₃ receptors (IP₃ R) and ryanodine receptors (RyR) to alter Ca²⁺ signalling in endothelial cells.

Experimental approach

We investigated the effects of FK506 and rapamycin on Ca²⁺ release via IP₃ R and RyR in hundreds of endothelial cells, using the indicator Cal-520, in intact mesenteric arteries from male Sprague-Dawley rats. I

SUBMITTER: Buckley C 

PROVIDER: S-EPMC7042112 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature