Abstract
Systemic hypertension, a pathological process to which the renin-angiotensin system contributes importantly, is characterized by a thrombophilic diathesis and an increased risk for acute ischemic coronary events. That apparently contradictory profile might, to some extent, relate to the modulating properties of Angiotensin II, the effector arm of the renin angiotensin system, on tissue factor expression, the physiologic initiator of blood coagulation and a basic mechanism in the pathogenesis of acute thrombosis. In fact, monocytes and macrophages within the atherosclerotic plaque as well as inflamed vascular endothelial cells may locally synthesize Angiotensin II. In turn, the peptide, by binding to its specific membrane receptors, activates a series of intracellular signals eventually converging upon NF-κB, a transcription factor that upregulates tissue factor expression. Drugs interfering with the renin-angiotensin system, either by inhibiting conversion of Angiotensin I to Angiotensin II or by blocking its receptors, have the potential to inhibit tissue factor expression and to modulate its procoagulant effect. This property may contribute to the protection exerted by renin-angiotensin blockers from acute ischemic events in patients with hypertension and other cardiovascular diseases.
Keywords: Renin angiotensin system, tissue factor, hypertension, acute coronary syndrome, NF-κB
Endocrine, Metabolic & Immune Disorders - Drug Targets
Title: Tissue Factor Modulation by Angiotensin II: A Clue to a Better Understanding of the Cardiovascular Effects of Renin-Angiotensin System Blockade?
Volume: 8 Issue: 4
Author(s): Alessandro Celi, Alessandra Del Fiorentino, Silvana Cianchetti and Roberto Pedrinelli
Affiliation:
Keywords: Renin angiotensin system, tissue factor, hypertension, acute coronary syndrome, NF-κB
Abstract: Systemic hypertension, a pathological process to which the renin-angiotensin system contributes importantly, is characterized by a thrombophilic diathesis and an increased risk for acute ischemic coronary events. That apparently contradictory profile might, to some extent, relate to the modulating properties of Angiotensin II, the effector arm of the renin angiotensin system, on tissue factor expression, the physiologic initiator of blood coagulation and a basic mechanism in the pathogenesis of acute thrombosis. In fact, monocytes and macrophages within the atherosclerotic plaque as well as inflamed vascular endothelial cells may locally synthesize Angiotensin II. In turn, the peptide, by binding to its specific membrane receptors, activates a series of intracellular signals eventually converging upon NF-κB, a transcription factor that upregulates tissue factor expression. Drugs interfering with the renin-angiotensin system, either by inhibiting conversion of Angiotensin I to Angiotensin II or by blocking its receptors, have the potential to inhibit tissue factor expression and to modulate its procoagulant effect. This property may contribute to the protection exerted by renin-angiotensin blockers from acute ischemic events in patients with hypertension and other cardiovascular diseases.
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Cite this article as:
Celi Alessandro, Fiorentino Del Alessandra, Cianchetti Silvana and Pedrinelli Roberto, Tissue Factor Modulation by Angiotensin II: A Clue to a Better Understanding of the Cardiovascular Effects of Renin-Angiotensin System Blockade?, Endocrine, Metabolic & Immune Disorders - Drug Targets 2008; 8 (4) . https://dx.doi.org/10.2174/187153008786848259
DOI https://dx.doi.org/10.2174/187153008786848259 |
Print ISSN 1871-5303 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3873 |
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