Key result
In the rat kidney in vivo, integrated renal hyperemic responses to ACh and bradykinin were blunted in diabetes due to impaired nitric oxide function.
Population
Rats (nondiabetic and established streptozotocin-induced diabetic models)
Comparison
Endothelium stimulation via locally administered… vs Nondiabetic rats vs. diabetic rats; baseline…
Design
Preclinical
Authors
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Preclinical rat data warrant no change in clinical diabetes care; leaves open translation of nitric oxide impairment to human renal outcomes.
In the rat kidney in vivo, nitric oxide dominates integrated hyperemic responses to ACh and bradykinin, and this endothelium-dependent vasodilation is impaired in diabetes due to diminished NO function.
Edgley et al. (2008) studied Streptozotocin-induced diabetes. Streptozotocin-induced diabetes vs. Nondiabetic rats was evaluated on Integrated renal hyperemic responses to ACh and bradykinin. In the rat kidney in vivo, integrated renal hyperemic responses to ACh and bradykinin were blunted in diabetes due to impaired nitric oxide function.
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