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Research Article Free access | 10.1172/JCI116043
Section on Pharmacology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.
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Section on Pharmacology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.
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Section on Pharmacology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.
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Section on Pharmacology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.
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Published November 1, 1992 - More info
Angiotensin II is a vasoactive peptide and may act as a growth factor in vascular smooth muscle cells. Experimental injury of the rat aorta causes rapid migration of medial smooth muscle cells and their proliferation resulting in the formation of neointima. We have examined, using quantitative autoradiography, the expression of angiotensin II receptor subtypes AT1 and AT2, and angiotensin-converting enzyme, in the neointima formed in the rat thoracic aorta 15 d after balloon-catheter injury. In contrast to the normal aortic wall, which contained both AT1 and AT2 receptors (80% and 20%, respectively), neointimal cells expressed almost exclusively angiotensin II AT1 receptors. The apparent number of these receptors was fourfold higher in the neointima compared to that in the normal aortic wall. The affinities of the neointimal receptors to angiotensin II or to the AT1 receptor antagonist, losartan, were not different from those in the normal aortic wall. Angiotensin-converting enzyme binding in the neointima was not different from that in the media of the uninjured aorta. Our data suggest that angiotensin II AT1 receptors may have a significant role in injury-induced vascular smooth muscle proliferation and migration.
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