Maintaining a balance between the vasorelaxor atheroprotective factors (prostacydin and nitric oxide) and vasoconstrictor pro-atherogenic factors (endothelin-1 and angiotensin II) is the basis of endothelial (79) When this balance is altered, the endothelium becomes dysfunctional and no longer able to prevent noxious stimuli, such as oxidized low-density lipoprotein (LDL) cholesterol, from breaching it, thus inciting inflammation and damaging underlying vascular architecture.
Angiotensin II induces production of superoxide radicals that scavenge nitric oxide; it also increases expression of endothelin-1.
85) Neither enalapril nor losartan (an angiotensin II type I receptor antagonist) improved endothelial function, suggesting that a tissue effect by bradykinin, and thus locally induced nitric oxide, may explain these findings.
40,67) Nitric oxide not only retards vasoconstriction but has been shown to decrease inflammation, platelet aggregation, and thrombosis (ie, actions opposite those of angiotensin II).
Studies involving animal and human subjects, in vitro and in vivo, have demonstrated effects of ACE inhibitors on angiotensin II and bradykinin at the cellular level, which may alter the initiation and progression of atherosclerosis.
Angiotensin II causes endothelial cell and vascular smooth muscle cell migration, growth, and proliferation; (39,61) it also stimulates cardiac fibroblast growth and hypertrophy.
An alternative strategy for the radioimmunoassay of angiotensin peptides using amino-terminal-directed antisera: measurement of eight angiotensin peptides in human plasma.
Specific measurement of angiotensin metabolites and in vitro generated angiotensin II in plasma.
Differential regulation of angiotensin peptide levels in plasma and kidney of the rat.
Aging and human hormonal and pressor responsiveness to angiotensin II infusion with simultaneous measurement of exogenous and endogenous angiotensin II.