Key result
Tempol augmented the Angiotensin II-induced AT2 receptor-mediated relaxation response in aortic rings from diabetic rats (80%) compared to baseline diabetic response (55%).
Why the study?
Does Tempol augment angiotensin II-induced AT2 receptor-mediated relaxation in the thoracic aorta of streptozotocin-induced diabetic rats?
Population
Thoracic aortic rings isolated from male Sprague-Dawley rats pretreated with streptozotocin or vehicle 8…
Comparison
Tempol added to Angiotensin II in the presence… vs Aortic rings from control rats, and diabetic…
Design
Preclinical
Follow-up
8 weeks (duration of diabetes prior to study)
Authors
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May inform AT2-targeted vascular therapies in diabetes; leaves open translation from this animal model.
Does Tempol augment angiotensin II-induced AT2 receptor-mediated relaxation in the thoracic aorta of streptozotocin-induced diabetic rats?
Absolute Event Rate: 80% vs 55%
Tempol augments AT2 receptor-mediated relaxation in the thoracic aorta of diabetic rats, suggesting a compensatory mechanism involving nitric oxide and ATP-sensitive K channels that could be therapeutically exploited.
ARUN et al. (2004) studied Streptozotocin-induced diabetes. Tempol vs. Vehicle/Control was evaluated on Angiotensin II-induced relaxation response (% relaxation). Tempol augmented the Angiotensin II-induced AT2 receptor-mediated relaxation response in aortic rings from diabetic rats (80%) compared to baseline diabetic response (55%).
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