Neointima formation after vascular injury is angiotensin II mediated.

Abstract

Smooth muscle proliferation of injured blood vessels leads to pathologically significant stenosis in animals and humans. We report here the pharmacological confirmation of an involvement of angiotensin II in this process as a major, necessary mediator of neointima formation. In the rat carotid artery, an animal model of post-angioplastic restenosis, we have obtained by local intraluminal infusion of peptidic angiotensin II antagonist after balloon catheterization, suppression of neointima formation and preservation of the luminal integrity. Sham operated control animals treated without medication and operated control animals treated simultaneously with angiotensin converting enzyme inhibitor and with agonistic angiotensin II, suffered major stenosis through the myoproliferative response of the injured vessel. These results prove that angiotensin II plays a key role as a mediator of vascular neointima formation.

• Authors: S Laporte, E Escher
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 187 Issue 3 Pg. 1510-6 (Sep 30 1992) ISSN: 0006-291X [Print] United States
• PMID: 1417827 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Angiotensin Receptor Antagonists
• Receptors, Angiotensin
• Angiotensin II
• Cilazapril

Topics

• Angiotensin II (analogs & derivatives, antagonists & inhibitors, physiology)
• Angiotensin Receptor Antagonists
• Animals
• Blood Pressure (drug effects)
• Catheterization (adverse effects)
• Cilazapril (pharmacology)
• Male
• Muscle Development
• Muscle, Smooth, Vascular (growth & development)
• Rats
• Rats, Sprague-Dawley
• Receptors, Angiotensin (drug effects, metabolism)
• Vascular Patency