Kinin B1 receptor: a potential therapeutic target in sepsis-induced vascular hyperpermeability.

ABSTRACT:

Background

In sepsis, the endothelial barrier becomes incompetent, with the leaking of plasma into interstitial tissues. VE-cadherin, an adherens junction protein, is the gatekeeper of endothelial cohesion. Kinins, released during sepsis, induce vascular leakage and vasodilation. They act via two G-protein coupled receptors: B1 (B1R) and B2 (B2R). B1R is inducible in the presence of pro-inflammatory cytokines, endotoxins or after tissue injury. It acts at a later stage of sepsis and elicits a sustained inflammatory response. The aim of our study was to investigate the relationships between B1R and VE-cadherin destabilization in vivo in a later phase of sepsis.

Methods

Experimental, prospective study in a university research laboratory. We used a polymicrobial model of septic

SUBMITTER: Ruiz S 

PROVIDER: S-EPMC7168845 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature