α-Toxin perfusion: a new method for selective impairment of endothelial function in isolated vessels or intact vascular beds
- 1 November 1995
- journal article
- Published by Canadian Science Publishing in Canadian Journal of Physiology and Pharmacology
- Vol. 73 (11) , 1669-1673
- https://doi.org/10.1139/y95-729
Abstract
We describe a method for selectively permeabilizing endothelial ceils, using the membrane pore forming exoprotein Staphylococcus aureus α-toxin. Experiments were performed in rabbit central ear artery or its main side branch under isometric conditions, on the isolated perfused kidney, or in cannulated pressurized renal arteries. In presence of α-toxin, endothelial-dependent vasodilator responses elicited by acetylcholine or A23187 were abolished, whereas the sensitivity of smooth muscle cells to constrictors (norepinephrine, phenylephrine, or KCl) or dilators (sodium nitroprusside) was not affected. The results indicate that restricting the α-toxin to the luminal surface induces selective impairment of vascular endothelial function. This method of eliminating endothelium-dependent vasodilator responses may prove to be useful in the study of endothelial – smooth muscle interactions of isolated small arteries and intact vascular beds.Key words: α-toxin, endothelium, vasodilation, vascular smooth muscle.Keywords
This publication has 6 references indexed in Scilit:
- Pore-forming bacterial toxins potently induce release of nitric oxide in porcine endothelial cells.The Journal of Experimental Medicine, 1993
- Protein kinase C modulates basal myogenic tone in resistance arteries from the cerebral circulation.Circulation Research, 1991
- Staphylococcal alpha toxin — recent advancesToxicon, 1988
- Cellular mechanisms underlying excitotoxicityTrends in Neurosciences, 1987
- Laser-induced endothelial damage inhibits endothelium-dependent relaxation in the cerebral microcirculation of the mouse.Circulation Research, 1987
- The requirement for endothelial cells in the relaxation of arteries by acetylcholine and some other vasodilatorsTrends in Pharmacological Sciences, 1981