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AJP - Heart and Circulatory Physiology, Vol 257, Issue 4 1315-H1320, Copyright © 1989 by American Physiological Society
ARTICLES |
J. L. Mehta, D. L. Lawson, W. W. Nichols and P. Mehta
Department of Medicine, University of Florida College of Medicine, Gainesville 32610.
To determine the influence of polymorphonuclear leukocytes (PMNLs) on vascular smooth muscle tone, isolated human PMNLs (10(4)-10(7) cells/ml) were suspended in a tissue bath with precontracted rat aortic rings with or without endothelium. PMNLs in low concentrations (10(4) and 10(5) cells/ml) caused a mild contraction, and in higher concentrations (10(6) and 10(7) cells/ml) caused a modest relaxation of aortic rings with intact endothelium. In contrast, PMNLs caused a potent concentration-dependent relaxation of deendothelialized rings (P less than 0.01 compared with rings with intact endothelium). The PMNL-induced vascular smooth muscle relaxation was abolished by both hemoglobin and methylene blue and potentiated by both superoxide dismutase and captopril. Although suspension of PMNLs caused release of eicosanoids, thromboxane A2 and prostacyclin, from rings with intact endothelium, neither indomethacin nor the TxA2-endoperoxide receptor antagonist SQ 29548 modified the effects of PMNLs on vascular smooth muscle tone. These observations suggest that unstimulated PMNLs generate a smooth muscle relaxant, which has biological characteristics similar to the endothelium-derived relaxing factor. Since the activity of this PMNL-derived smooth muscle relaxant is more pronounced in deendothelialized vascular segments, it appears that endothelium provides a barrier against vasorelaxation by high concentrations of PMNLs.
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J. L. Hart-Favaloro and O. L. Woodman Rabbit polymorphonuclear leukocytes release a factor that causes constriction of the coronary vasculature Am J Physiol Heart Circ Physiol, October 1, 1998; 275(4): H1322 - H1328. [Abstract] [Full Text] [PDF] |
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