Hydrogen sulfide donor AP123 restores endothelial nitric oxide-dependent vascular function in hyperglycemia via a CREB-dependent pathway.

ABSTRACT: Diabetes is associated with severe vascular complications involving the impairment of endothelial nitric oxide synthase (eNOS) as well as cystathionine γ-lyase (CSE) activity. eNOS function is suppressed in hyperglycaemic conditions, resulting in reduced NO bioavailability, which is paralleled by reduced levels of hydrogen sulfide (H₂S). Here we have addressed the molecular basis of the interplay between the eNOS and CSE pathways. We tested the impact of H₂S replacement by using the mitochondrial-targeted H₂S donor AP123 in isolated vessels and cultured endothelial cells in high glucose (HG) environment, at concentrations not causing any vasoactive effect per se. Aorta exposed to HG displayed a marked reduction of acetylcholine (Ach)-induced vasorelaxation

SUBMITTER: Montanaro R 

PROVIDER: S-EPMC10025109 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature