Effects of Superoxide Dismutase on Changes in EDRF-and EDHF-Mediated Relaxation of Diabetic Rat Aortas Exposed to Oxygen Free Radicals.
- Author:
Dong Hee KIM
;
Ye Kyung SEO
;
Jik Hwa NAM
;
Byung Ho SIN
;
Jung Guk KIM
;
Sung Woo HA
;
Bo Whn KIM
- Publication Type:Original Article
- Keywords:
Diabetic rat aorta;
EDRF;
EDHF;
Oxygen free radical;
SOD
- MeSH:
Acetylcholine;
Animals;
Aorta*;
Blood Vessels;
Endothelium;
Endothelium-Dependent Relaxing Factors;
Free Radicals*;
Norepinephrine;
Oxygen*;
Rats*;
Relaxation*;
Superoxide Dismutase*;
Superoxides*
- From:Journal of Korean Society of Endocrinology
1997;12(2):265-274
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The relaxative response of blood vessels to acetylcholine (ACh) is known to be abnormal in diabetic rat due to changes in endothelium-derived relaxing factor (EDRF) and/or endothelium-derived hyperpolarizing factor (EDHF)-mediated action. Oxygen free radical (OFR) interferes with endothelium dependent relaxation to ACh in diabetic rats; this effect rnay be prevented by superoxide dismutase (SOD), OFR scavenger. Then, we determined the effect of SOD on modulation of OFR-induced damage to EDRF and EDHF-mediated relaxations to ACh in diabetic rat aortas. METHODS: After aortas were incubated with free radical generating system for 15 min with or without SOD pretreatment (150 U/mL) and contracted submaximally by norepinephrine (10 (-5) M), relaxative responses to cumulative concentrations (10 (-9) M to 10 (-5) M) of ACh were measured in aortas isolated from the control and 6-8 week streptozotocin-induced diabetic rat. We measured relaxative responses to ACh in these aortas treated with calmidazolium (100uM) or N-nitro-L-arginine methyl ester (luM) after exposure to OFR with/without SOD pretreatment, RESULTS: The ACh-induced relaxation (10 (-9)M to 10 (-5) M) was significantly decreased in diabetic than in control rat aortas (p<0.05). ACh-induced relaxation in diabetic rat aortas was significantly impaired from 79.3% to 71.2% after exposure to OFR (p<0.05), and the degree of ACh-induced relaxation was recovered from 71.2% to 84.0% after pretreatment with SOD (p<0.05). EDRF-mediated relaxation to ACh in diabetic rat aortas was significantly impaired from 71.2% to 61.6% after exposure to OFR (p<0.05), and the degree of impairment of ACh-induced EDRF-mediated relaxation was recovered from 61.6% to 76.0% after pretreatment with SOD. After exposure to OFR, EDHF-mediated relaxation to ACh in diabetic rat aortas was not significanlty impaired. However, the degree of impairment of EDHF-mediated relaxation to ACh was recovered from 46.0% to 59.5% after pretreatment with SOD. CONCLUSION: This study suggests that OFR may impair mainly EDRF-mediated relaxation to ACh and SOD may protect rnainly OFR-induced damage to EDRF-mediated relaxation to ACh in diabetic rat aortas.
