Impaired endothelium-dependent relaxation is mediated by reduced production of nitric oxide in the streptozotocin-induced diabetic rats.
- Author:
Kyoung Sook PARK
1
;
Cuk Seong KIM
;
Sang Won KANG
;
Jin Bong PARK
;
Kwang Jin KIM
;
Seok Jong CHANG
;
Byeong Hwa JEON
Author Information
1. Department of Physiology, College of Medicine, Chungnam National University, Taejon, Korea.
- Publication Type:Original Article
- MeSH:
Acetylcholine;
Animals;
Aorta;
Blotting, Western;
Endothelial Cells;
Indomethacin;
Nitric Oxide Synthase;
Nitric Oxide Synthase Type III;
Nitric Oxide*;
Nitroprusside;
Norepinephrine;
Plasma;
Rats*;
Rats, Sprague-Dawley;
Relaxation*;
Streptozocin
- From:The Korean Journal of Physiology and Pharmacology
2000;4(3):263-270
- CountryRepublic of Korea
- Language:English
-
Abstract:
To evaluate the involvement of nitric oxide production on the endothelium-dependent relaxation in diabetes, we have measured vascular and endothelial function and nitric oxide concentration, and the expression level of endothelial nitric oxide synthase in the streptozotocin-induced diabetic rats. Diabetic rats were induced by the injection of streptozotocin (50 mg/kg i.v.) in the Sprague-Dawley rats. Vasoconstrictor responses to nonrepinephrine (NE) showed that maximal contraction to norepinephrine (10(-5) M) was significantly enhanced in the aorta of diabetic rats. Endothelium-dependent relaxation induced by acetylcholine was markedly impaired in the aorta of diabetic rats, these responses were little improved by the pretreatment with indomethacin. However, endothelium-independent relaxation induced by nitroprusside was not altered in the diabetic rats. Plasma nitrite and nitrate (NO2/3) levels in diabetic rats were significantly lower than innon-diabetic rats. Western blot analysis using a monoclonal antibody against endothelial cell nitric oxide synthase (eNOS) revealed that the protein level was lower in the aorta of diabetic rats than in non-diabetic rats. These data indicate that nitric oxide formation and eNOS expression is reduced in diabetes, and this would, in part, account for the impaired endothelium-dependent relaxation in the aorta of streptozotocin-induced diabetic rats.
