PTPRG is an ischemia risk locus essential for HCO₃^--dependent regulation of endothelial function and tissue perfusion.

ABSTRACT: Acid-base conditions modify artery tone and tissue perfusion but the involved vascular-sensing mechanisms and disease consequences remain unclear. We experimentally investigated transgenic mice and performed genetic studies in a UK-based human cohort. We show that endothelial cells express the putative HCO₃^--sensor receptor-type tyrosine-protein phosphatase RPTPγ, which enhances endothelial intracellular Ca²⁺-responses in resistance arteries and facilitates endothelium-dependent vasorelaxation only when CO₂/HCO₃^- is present. Consistent with waning RPTPγ-dependent vasorelaxation at low [HCO₃^-], RPTPγ limits increases in cerebral perfusion during neuronal activity and augments decreases in cerebral perfus

SUBMITTER: Hansen KB 

PROVIDER: S-EPMC7541084 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature