Abstract
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► We have shown for the first time that CA administration protects from diabetes induced hypertension. ► We have shown that this protective effect is mediated, at least in part, by preventing the alterations in vascular function. ► This suggests a novel biological activity for the well tolerated natural compound, cinnamaldehyde in diabetes complications.
Here we investigated cinnamaldehyde (CA) effect on diabetes-induced hypertension. Insulin deficiency was induced by streptozotocin while, insulin resistance by fructose. Rats were left 8weeks or 12weeks after STZ or fructose administration respectively. CA (20mgkg−1day−1) was daily administered in the last 6weeks. Then, blood pressure (BP) was recorded. Isolated Aorta reactivity to phenylephrine (PE), KCl, acetylcholine (ACh) was studied as well as nitric oxide (NO) generation plus Ca2+ influx. Insulin deficiency was associated with elevated BP, increased response to PE and KCl, decreased response to ACh and impaired NO generation. CA treatment prevented hyperglycemia and its associated impaired vascular reactivity. Insulin resistance was associated with elevated BP while, CA prevented this elevation. Insulin resistance increased response to PE and KCl, decreased response to ACh, while CA treatment normalized response to KCl and PE but not to ACh. Insulin resistance was accompanied with reduced NO generation but exaggerated Ca2+ influx while CA restored normal Ca2+ influx but did not affect NO generation. In conclusion, CA prevents development of hypertension in insulin deficiency and insulin resistance through normalization of vascular contractility in addition to its insulinotropic effect in insulin deficiency.