Study of the activity of endothelial cell nitric oxide synthase in mouse models for atherosclerosis.

Hypercholesterolemia and other risk factors for atherosclerosis lead to decreased bioavailability of nitric oxide (NO) in humans. Yet, the receptor-stimulated activity of endothelial nitric oxide synthase (eNOS) remains undisturbed in isolated aortas of hypercholesterolemic apolipoprotein E deficient (apoE-/-) mice before plaque formation. Bioavailability of "basal" NO, i.e. without agonists for endothelial cell (EC) receptors is, however, compromised in young apoE-/- mice. In this project, we will investigate whether the discrepancy between "basal" and receptor-mediated NO availability is due to mechanical factors, such as shear forces.

Keywords:MICE MODEL, PHARMACOLOGY, ATHEROSCLEROSIS

Disciplines:Cardiac and vascular medicine, Physiology, Biomarker discovery and evaluation, Drug discovery and development, Medicinal products, Pharmaceutics, Pharmacognosy and phytochemistry, Pharmacology, Pharmacotherapy, Toxicology and toxinology, Other pharmaceutical sciences