@article{APS7314,
author = {Xun Guo and Wen-Lan Liu and Li-Wei Chen and Zhao-Gui Guo},
title = {High glucose impairs endothelium-dependent relaxation in rabbit aorta},
journal = {Acta Pharmacologica Sinica},
volume = {21},
number = {2},
year = {2016},
keywords = {},
abstract = {\"AIM:
To study the effects of high glucose on endothelium-dependent relaxation (EDR) and the action of L-arginine, superoxide dismutase (SOD), or glucose re-normalization in aorta.
METHODS:
Measurement of EDR of the isolated rabbit thoracic aortic rings.
RESULTS:
Elevated glucose (25 mmol.L-1) caused profound impairment of acetylcholine (ACh)-induced relaxation, EC50: 1.6 mumol.L-1 (95% CL: 7.9 nmol.L(-1)-6.3 mumol.L-1) vs normal glucose (5.5 mmol.L-1) EC50: 0.08 mumol.L-1 (95% CL: 0.02 mumol.L(-1)-0.3 mumol.L-1) (P < 0.01), which not reversed followed by a further 24 h incubation in normal glucose M199, EC50: 2.0 mumol.L-1 (95% CL: 0.2 pmol.L(-1)-12.5 mumol.L-1). However, aortic rings incubated with mannitol (19.5 mmol.L-1) relaxed to ACh normally. L-arginine 1 mmol.L-1 or SOD 150 U.L-1 restored ACh relaxation in elevated glucose to normal, EC50: 0.16 mumol.L-1 (95% CL: 0.04 mumol.L(-1)-0.8 mumol.L-1) and 0.16 mumol.L-1 (95% CL: 0.03-0.63 mumol.L-1). The relaxation in response to sodium nitroprusside was not different between rings exposed to normal or elevated glucose.
CONCLUSION:
Hyperglycemia impaired EDR, which was not reversible by glucose re-normalization, increased free radical production and altered L-arginine metabolism were involved in this endothelium dysfunction.\"},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/7314}
}