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Am J Physiol Lung Cell Mol Physiol 275: L756-L763, 1998;
1040-0605/98 $5.00
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Vol. 275, Issue 4, L756-L763, October 1998

Involvement of cytochrome P-450 enzyme activity in the control of microvascular permeability in canine lung

Claire L. Ivey1, Alan H. Stephenson2, and Mary I. Townsley1

1 Department of Physiology, University of South Alabama, Mobile, Alabama 36688; and 2 Department of Pharmacological and Physiological Science, St. Louis University School of Medicine, St. Louis, Missouri 63104

Products of cytochrome P-450 enzymes may play a role in capacitative Ca2+ entry in endothelial cells, which can promote a rise in vascular permeability. Thapsigargin (150 nM) stimulated capacitative Ca2+ entry and increased the capillary filtration coefficient (Kf,c) in isolated normal canine lung lobes. Pretreatment of the lobes with cytochrome P-450 inhibitors clotrimazole (10 µM) or 17-octadecynoic acid (5 µM) abolished the thapsigargin-induced increases in Kf,c. Because clotrimazole also blocks Ca2+-activated K+ channels, the K+-channel blocker tetraethylammonium (10 mM) was used to ensure that permeability was not influenced by this mechanism. Tetraethylammonium did not affect thapsigargin-induced permeability. The effects of the cytochrome P-450 arachidonic acid metabolite 5,6-epoxyeicosatrienoic acid (EET) were also investigated in lobes taken from control dogs and dogs with pacing-induced heart failure (paced at 245 beats/min for 4 wk). 5,6-EET (10 µM) significantly increased Kf,c in lobes from the control but not from the paced animals. We conclude that cytochrome P-450 metabolites are involved in mediating microvascular permeability in normal canine lungs, but an absence of 5,6-EET after heart failure does not explain the resistance of lungs from these animals to permeability changes.

capacitative calcium entry; epoxyeicosatrienoic acid; pulmonary endothelium; congestive heart failure; capillary filtration coefficient


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