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Pertussis toxin relaxes small arteries with no vascular lesions or vascular smooth muscle cell injury.

Authors :
van Meijeren CE
Vleeming W
Dormans JA
van de Kuil T
Opperhuizen A
Hendriksen CF
de Wildt DJ
Source :
Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie [Exp Toxicol Pathol] 2004 Dec; Vol. 56 (3), pp. 139-43.
Publication Year :
2004

Abstract

Previous studies showed that pertussis toxin (PT) decreased agonist-induced contractions of isolated rat small mesenteric resistance arteries independently from endothelium, nitric oxide-synthase or intracellular calcium concentrations. In this study, it was investigated if the PT-induced decreased contractile properties of small mesenteric resistance arteries could be a consequence of a PT-induced vascular and/or smooth muscle cell injury, leading to loss of contractile functionality. Male Wistar rats were treated with PT (30 microg/kg, intravenously) and sections of isolated small mesenteric resistance arteries were investigated with light- and electron microscopy. Light microscopic investigation of cross-sectioned small mesenteric resistance arteries of control animals clearly showed a contracted phase, while PT-pretreated animals showed a relaxed smooth inner surface of the vessel, indicating a vasodilated state. Electron microscopic investigation showed that PT-pretreatment neither induced vascular lesions nor caused morphological or numerical changes in cell organelles such as contractile elements of vascular smooth muscle cells. In conclusion, the PT-induced decreased contractile properties of isolated rat small resistance arteries are not caused by a PT-induced vascular and/or smooth muscle cell injury.

Details

Language :
English
ISSN :
0940-2993
Volume :
56
Issue :
3
Database :
MEDLINE
Journal :
Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie
Publication Type :
Academic Journal
Accession number :
15625782
Full Text :
https://doi.org/10.1016/j.etp.2004.07.003