TY - JOUR
T1 - Effects of the superoxide dismutase mimetic tempol on impaired endothelium-dependent and endothelium-independent relaxations in type II diabetic rats
AU - Oniki, Hideyuki
AU - Goto, Kenichi
AU - Fujii, Koji
AU - Kansui, Yasuo
AU - Murakami, Noboru
AU - Ohtsubo, Toshio
AU - Matsumura, Kiyoshi
AU - Kitazono, Takanari
N1 - Funding Information:
Declaration of interest: This work was supported in part by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (07307010, 13670722), Tokyo, Japan. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
PY - 2013
Y1 - 2013
N2 - Endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization and relaxation, and endothelium-independent relaxations to the nitric oxide donor sodium nitroprusside and the adenosine 5′-triphosphate (ATP)-sensitive K+-channel opener levcromakalim were both impaired in mesenteric arteries of type II diabetic Goto-Kakizaki rats. The treatment with the superoxide dismutase mimetic tempol or its combination with the angiotensin II type 1 receptor blocker candesartan failed to improve EDHF-mediated responses, although both treatments partially improved endothelium-independent relaxations. These findings suggest that increased oxidative stress may in part account for the impaired endothelium-independent relaxations in diabetes, while it does not play a major role in the impaired EDHF-mediated responses.
AB - Endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization and relaxation, and endothelium-independent relaxations to the nitric oxide donor sodium nitroprusside and the adenosine 5′-triphosphate (ATP)-sensitive K+-channel opener levcromakalim were both impaired in mesenteric arteries of type II diabetic Goto-Kakizaki rats. The treatment with the superoxide dismutase mimetic tempol or its combination with the angiotensin II type 1 receptor blocker candesartan failed to improve EDHF-mediated responses, although both treatments partially improved endothelium-independent relaxations. These findings suggest that increased oxidative stress may in part account for the impaired endothelium-independent relaxations in diabetes, while it does not play a major role in the impaired EDHF-mediated responses.
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U2 - 10.3109/10641963.2012.702829
DO - 10.3109/10641963.2012.702829
M3 - Article
C2 - 22783963
AN - SCOPUS:84875694164
VL - 35
SP - 112
EP - 119
JO - Clinical and Experimental Hypertension
JF - Clinical and Experimental Hypertension
SN - 1064-1963
IS - 2
ER -
