Endothelial dysfunction is associated to traditional cardiovascular risk factors, such as hypertension. In spontaneously hypertensive rats (SHR), an essential hypertension model, the endothelial dysfunction, evaluated as a reduction of endothelium-dependent relaxation, is attributed to increased vasoconstrictor prostanoids. Reduced dehydroepiandrosterone (DHEA) levels exhibit an inverse correlation with increased cardiovascular risk. DHEA stimulates the nitric oxide production and reduces the bioavailability of reactive oxygen species, which can represent at least part of the mechanisms involved in DHEA cardioprotective effects. Despite the fact that DHEA reduces vasoconstrictor prostanoid release in an insulin resistance/hypertension model, it is still unknown whether DHEA could improve the vascular function in models, such as SHR, in which endothelial dysfunction is attributable to increased vasoconstrictor prostanoids.Therefore, the aim of the present project is to evaluate the effects of DHEA on the endothelium-dependent relaxation in the aorta of SHR, with emphasis on cyclooxygenase products.
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