Key result
Treatment with tempol or its combination with candesartan failed to improve EDHF-mediated responses but partially improved endothelium-independent relaxations in type II diabetic rats.
Why the study?
Does tempol or its combination with candesartan improve impaired endothelium-dependent and endothelium-independent relaxations in type II diabetic rats?
Does tempol or its combination with candesartan improve impaired endothelium-dependent and endothelium-independent relaxations in type II diabetic rats?
Increased oxidative stress may partially account for impaired endothelium-independent relaxations in diabetes, but does not play a major role in impaired EDHF-mediated responses.
Does not support tempol for EDHF impairment in diabetic rats; leaves open partial oxidative stress role in endothelium-independent dysfunction.
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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Oniki et al. (2012) studied Type II diabetes. Tempol or tempol + candesartan was evaluated on EDHF-mediated responses and endothelium-independent relaxations. Treatment with tempol or its combination with candesartan failed to improve EDHF-mediated responses but partially improved endothelium-independent relaxations in type II diabetic rats.
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