Does endothelin-1 but not angiotensin II contribute to functional aging in murine carotid arteries?
Aging in carotid arteries decreases ETA receptor gene expression and responsiveness to ET-1, which nevertheless becomes increasingly dependent upon NAPDH oxidase activity with age; responses to Ang II and gene expression of its receptors are however unaffected. These findings suggest that physiological aging differentially regulates functional responses to G protein-coupled receptor agonists and the signaling pathways associated with their activation.
An assessment of the data on the risk factors for ischaemic heart disease and mortality suggests that most of the decline in mortality from ischaemic heart disease can be explained by changes in the three main coronary risk factors.