![]() In agreement with this, our results show that the administration of L-arginine plus nor-NOHA increases the response to acetylcholine in the aorta from old WT mice. Moreover, arginase inhibitors restore NO-mediated vasodilation in rats and in elderly subjects. In aging, arginase upregulation contributes to endothelial dysfunction. ![]() Although all these hallmarks are very useful for predicting patients’ biological age, they need to be combined to develop an effective biomarker. Finally, vascular calcifications are observed in cells of the media or intima of the arterial wall in aging. Moreover, there is positive feedback between arterial stiffness and hypertension that is closely related to endothelial dysfunction. They cause reduced vascular compliance and increased arterial pressure. Some of the most remarkable vascular aging biological characteristics are elastin fragmentation and collagen accumulation. Vascular aging is a gradually developing process characterized by age-related alterations in both the structural and mechanical properties of the vascular wall, accompanied by functional vascular changes leading to the loss of arterial elasticity, reduced arterial compliance and endothelial dysfunction. Particularly, arteries suffer numerous detrimental processes, which could be considered as vascular aging hallmarks. Vascular aging has been identified as a cardiovascular risk factor. We conclude that the overexpressing G6PD mouse is a model to improve vascular health via the arginase pathway. Moreover, histological analyses demonstrated that age causes a thickness of aortic walls, but this did not occur in G6PD-Tg mice. Mice overexpressing G6PD underexpressed arginase II and also displayed a lower activity of this enzyme. ![]() Endothelial dysfunction was reverted by nor-NOHA, an arginase inhibitor. Vascular reactivity results showed a reduced acetylcholine-dependent relaxation in the old WT but not old G6PD-Tg group. For this study, three groups of male mice were used: young wild type (WT) (6–9 months), old WT (21–22 months) and old G6PD-Tg (21–22 months) mice. ![]() Our hypothesis is that glucose 6-P dehydrogenase (G6PD) overexpression could improve the endothelial function modulating the arginase pathway in aorta from mice. This enzyme competes with the endothelial nitric oxide synthase (eNOS) for L-arginine substrate. The increase of vascular arginase activity during aging causes endothelial dysfunction. ![]()
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