Partial escape of angiotensin converting enzyme (ACE) inhibition during prolonged ACE inhibitor treatment: Does it exist and does it affect the antihypertensive response?
Pathways for angiotensin II generation in intact human tissue: Evidence from comparative pharmacological interruption of the renin system.
Systematic review of combined angiotensin-converting enzyme inhibition and angiotensin receptor blockade in hypertension.
Compared with these vasoactive pathways, the angiotensin II-A[T.
This is the first demonstration that PM-induced vascular effects may be mediated by the angiotensin signaling.
Interaction of a non-peptide agonist with angiotensin II AT1 receptor mutants.
Immunohistochemical studies of atherosclerotic lesions within human coronary arteries have confirmed that significant sources of tissue ACE and angiotensin II are within regions of inflammatory cells, especially areas of clustered macrophages, as well as microvessel endothelial cells.
Some studies have demonstrated that the potent inhibition in angiotensin II generation early on with ACE inhibitors may wear off within weeks; angiotensin II may be generated by non-ACE pathways directly or indirectly.
By shifting the balance between angiotensin II and bradykinin, ACE inhibitors may modulate their various vascular effects (Fig.
Specific activity of the detection angiotensin was 1500-2200 pCi/fmol, i.
The generation and metabolization of angiotensin peptides after specimen sampling is a major problem, and enzyme inhibition before peptide measurement is crucial (11-13).
The sensitivity of our antiserum and its low cross-reactivity of <1% with other angiotensin peptides made it possible to reliably measure low endogenous Ang-(1-7) concentrations in blood even without additional HPLC.