Essential hypertension is associated with endothelial dysfunction and reactive oxygen species are considered to play a role here. But whether endothelial superoxide anion radical (O2-•) may play a role in the early development of hypertension remains uncertain. The aim of this study is to investigate whether endothelial nitric oxide synthase (eNOS)-derived endothelial oxidative stress is involved in the regulation of systolic blood pressure.
Oxidative stress generated by endothelial-specific expression of genetically destabilized C101A-eNOS selectively prevents the systolic blood pressure-reducing activity of vascular eNOS, while having no effect on aortic endothelium-dependent relaxation. These data suggest that a decrease of eNOS dimer stability associated with increased vascular oxidative stress in the microvascular endothelium might directly contribute to the regulation of blood pressure and may play a role in the development of essential hypertension.
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