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Abstract

Research on the development of atherosclerotic plaque and the mechanisms of acute coronary syndromes has identified multiple levels of input from the Renin Angiotension System. Drugs that block the Type I receptor for ANG II have joined ACE inhibitors as effective strategies to protect patients with atherosclerotic vascular disease as well as hypertensive and diabetic renal disease.

This vascular protection may be attributable to inhibition of the mitogenic effects of Angiotensin II, thus reducing ventricular and vascular hypertrophy. Yet many authorities now attribute this benefit to the improvement in endothelial dysfunction. The prime mechanism may be inhibition of NADH and NADPH oxidases, which then curtails production of reactive oxygen species. Thus preventing activation of transcriptional factors such as Nf-κB and initiation of the inflammatory cascade, (an obligatory part of the plaque development as well as its eventual destabilization). Recent reports have examined the independent effects of Type I and Type II Angiotensin receptors on inflammatory cytokines and plaque development and confirmed the role of the Type II receptor.

Clinical studies have validated the antihypertensive effects of blocking the type I receptor for angiotensin II. By also regressing left ventricular hypertrophy, this therapeutic intervention has impacted a formidable risk factor for stroke and myocardial infarction. The data from ValHeFT is a further indication of the benefit that can be expected from incorporating ANG II receptor blockade in the treatment of patients with left ventricular dysfunction. We have also learned of the benefit of Angiotensin II blockade in hypertensive patients with Type 2 DM and renal insufficiency. Studies presented last year at these meetings documented a renal protective effect that had not been validated in primary outcome studies with ACE inhibitors.

The potential of coming ACEI's and ARB's in patients at atherosclerotic risk is now under active investigation, along with studies on the interdependence of receptors for ANG II and oxidized LDL. This talk will focus on the newer aspects of Angiotensin II inhibition.

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© American Journal of Hypertension, Ltd. 2002
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