Have library access?
IP:18.97.14.82
  • Journals
  • OpenAccess

Age-related Endothelial Cell Senescence-Implications in Hypertension

Abstracts


Hypertension has remarkable influences on the decline of endothelial function. The involvement of nitric oxide (NO) bioavailability in hypertension, aging, or other cardiovascular diseases has been extensively reviewed. However, few studies have precisely identified whether the process of aging additively affected endothelial dysfunction in hypertension and its underlying mechanisms remained unclear. Participation of endothelial insulin and insulin-like growth factor-1 (IGF-1) signaling in vasorelaxation reactions via triggered phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT) expression is now well documented. Recently, we firstly confirmed that hypertension was the primary factor that caused the age-related endothelial senescence and affected endothelial dysfunction, but hypertension was not exacerbated in aging hypertensive rats. The process of aging induced worse endothelial insulin- and IGF-1-mediated vasorelaxation in hypertension, which was mainly attributed to the impaired activation of endothelial NO synthase (eNOS) and PI3K. Moreover, we further examined whether absence of antioxidant activities affected endothelial dysfunction. As a result, aging hypertensive rats manifested an increased oxidative stress, e.g. malondialdehyde concentration, and a decreased antioxidant activities, e.g. catalase activity and total antioxidant capacity, as well as decreased NO production. Thus, we provided novel lines of evidence to suggest aging additively affected insulin- and IGF-1-mediated endothelial dysfunction, partly caused by the impairment of endothelial PI3K-NOS-NO pathway. Also, the possibility that some part of aging-related endothelial dysfunction was attributed to the reduced NO production and imbalance of oxidative and antioxidant activities in hypertension was supported by our work.

Read-around