Abstract
Hypercholesterolemia and an activated renin-angiotensin-aldosterone system are well-established independent cardiovascular risk factors. Several lines of evidence support an important role of modified LDLs and angiotensin II in the development and progression of atherosclerosis. Angiotensin II is not only a potent vasoconstrictor, but it also promotes proinflammatory and prothrombotic properties of vascular cells. A growing body of in vitro studies shows the induction of cellular adhesion molecules and cytokines by angiotensin II in endothelial cells.1 In vivo, angiotensin II promotes leukocyte–endothelial cell interaction in the microcirculation. This proinflammatory mechanism involves the redox-sensitive mobilization of adhesion molecules such as P-selectin.2,3 These and several additional findings in cell systems and large vessels support a crucial role of the angiotensin II type-1 (AT1) receptor–mediated formation of reactive oxygen species (ROS) in the pathogenesis of atherosclerosis.4,5 However, the impact of AT1 receptor antagonism on the accelerated inflammatory and thrombotic response and ROS formation by hypercholesterolemia has not been studied in the microvasculature in vivo so far. In this issue of Hypertension , Petnehazy et al provide experimental evidence for the …
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
