Abstract
Mechanical forces and the activation of the renin-angiotensin system (RAS) may alter the NO/O2(*-) balance, imparing endothelial nitric oxide (NO) availability. This study investigates the link between RAS and NO/O2(*-) balance in human aortic endothelial cells (HAEC) exposed to pulsatile stretch with and without ACE inhibitor quinaprilat or angiotensin II type 1 (AT(1)) receptor antagonist losartan. Pulsatile stretch increased Ang II levels and O2(*-) production, reducing NO release. RAS blockade with quinaprilat or losartan restored the balance between NO and O2(*-). These results provide a molecular basis for understanding the vascular protective effects of ACE inhibition and AT(1) receptor antagonism.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Angiotensin II / metabolism*
-
Angiotensin II Type 1 Receptor Blockers / pharmacology*
-
Angiotensin-Converting Enzyme Inhibitors / pharmacology*
-
Biomechanical Phenomena
-
Cells, Cultured
-
Endothelial Cells / drug effects*
-
Endothelial Cells / metabolism
-
Endothelial Cells / physiology*
-
Hemorheology
-
Humans
-
Losartan / pharmacology
-
Models, Biological
-
Nitric Oxide / metabolism
-
Nitric Oxide Synthase Type III / metabolism
-
Oxidative Stress*
-
Pulsatile Flow
-
Renin-Angiotensin System / drug effects
-
Renin-Angiotensin System / physiology
-
Stress, Mechanical
-
Superoxides / metabolism
-
Tetrahydroisoquinolines / pharmacology
Substances
-
Angiotensin II Type 1 Receptor Blockers
-
Angiotensin-Converting Enzyme Inhibitors
-
Tetrahydroisoquinolines
-
Superoxides
-
Angiotensin II
-
Nitric Oxide
-
quinaprilat
-
NOS3 protein, human
-
Nitric Oxide Synthase Type III
-
Losartan