Deletion of endothelial arginase 1 does not improve vasomotor function in diabetic mice.

ABSTRACT: Endothelial arginase 1 was ablated to assess whether this prevents hyperglycemia-induced endothelial dysfunction by improving arginine availability for nitric oxide production. Endothelial Arg1-deficient mice (Arg1-KO^Tie2 ) were generated by crossing Arg1^fl/fl (controls) with Tie2Cre^tg/- mice and analyzed by immunohistochemistry, measurements of hemodynamics, and wire myography. Ablation was confirmed by immunohistochemistry. Mean arterial blood pressure was similar in conscious male control and Arg1-KO^Tie2 mice. Depletion of circulating arginine by intravenous infusion of arginase 1 or inhibition of nitric oxide synthase activity with L-N^G -nitro-arginine methyl ester increased mean arterial pressure similarly in

SUBMITTER: Chennupati R 

PROVIDER: S-EPMC5995309 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature