BALLOON ANGIOPLASTY AND INDUCTION OF NON-ENDOTHELIAL NITRIC-OXIDE SYNTHASE IN RABBIT CAROTID ARTERIES

Citation
Jm. Bosmans et al., BALLOON ANGIOPLASTY AND INDUCTION OF NON-ENDOTHELIAL NITRIC-OXIDE SYNTHASE IN RABBIT CAROTID ARTERIES, European journal of pharmacology, 310(2-3), 1996, pp. 163-174
Citations number
53
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00142999
Volume
310
Issue
2-3
Year of publication
1996
Pages
163 - 174
Database
ISI
SICI code
0014-2999(1996)310:2-3<163:BAAION>2.0.ZU;2-I
Abstract
The purpose of the study was to evaluate whether balloon angioplasty i s associated with changes in nitric oxide synthase (NO synthase) activ ity. Normal rabbit carotid arteries were examined 10 min or 1, 2, 3 or 10 weeks after angioplasty with 2 or 2.5-mm balloons. Immunohistology was used to evaluate intimal thickening and endothelial cell regenera tion. The NO synthase activity was studied functionally using isolated segments in organ chambers. Immunohistochemistry of the endothelial c ell markers von Willebrand factor and platelet endothelial cell adhesi on molecule-1 indicated that the regeneration of endothelial cells fro m patchy islands that remained after angioplasty was virtually complet e within 2 weeks. However, the endothelium-dependent relaxations elici ted by acetylcholine remained impaired up to 10 weeks after dilatation . Contractions elicited by 5-hydroxytryptamine (5-HT) were attenuated, but were significantly augmented by the NO synthase blocker, nitro-L- arginine. Furthermore, in contrast to normal arteries, the balloon-tre ated arteries developed marked contractions in response to nitro-L-arg inine methyl ester (L-NAME), contractions which could be reversed by L -arginine. The latter contractions and relaxations were not influenced by endothelial removal. These results suggest that although the endot helium quickly regenerates after severe balloon injury, the endotheliu m-dependent release of nitric oxide remains disturbed. However, the fu nctional data also suggest that angioplasty led to a significant induc tion of NO synthase in 'non-endothelial' cells of the artery.