INTERACTION OF NEUTROPHILS WITH VASCULAR SMOOTH-MUSCLE - IDENTIFICATION OF A NEUTROPHIL-DERIVED RELAXING FACTOR

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  • 1 April 1988
    • journal article
    • research article
    • Vol. 245  (1) , 102-111
Abstract
Experiments were designed to study the interaction of rat peritoneal neutrophils with the vascular smooth muscle of the rat aorta. Rings of aorta, suspended in 10-ml organ chambers containing a physiologic salt solution, were precontracted with phenylephrine. Neutrophils (1 .times. 105-4 .times. 107 cells/organ chamber) caused a cell number-dependent relaxation of the rat aorta that was augmented by superoxide dismutase (100 U/ml) or changing the oxygen content from 95 to 21%. The neutrophil-induced smooth muscle relaxation occurred in rings with and without endothelium and in rings precontracted with increasing concentrations of phenylephrine, prostaglandin F2.alpha. or KCl. Catalase (1000 U/ml) and mannitol (1 .times. 10-3 M) did not block the neutrophil-induced relaxation, whereas phenazine methosulfate (1 .times. 10-5 M), hydroquinone (3 .times. 10-5 M) and methylene blue (1 .times. 10-5 M) reversed the neutrophil-induced relaxation. Pre-exposure of endothelium-rubbed rings to neutrophils (2 .times. 107 cells/organ chamber; 15 min) depressed the subsequent concentration-response curve to phenylephrine but augmented the relaxation induced by the phosphodiesterase inhibitor zaprinast (1 .times. 10-5 M). The effluent from a column restraining the neutrophils induced a relaxation of endothelium-rubbed aortic rings that was prevented by methylene blue (1 .times. 10-5 M). These results demonstrate that rat neutrophils release a factor that has a pharmacologic profile similar to that previously reported for the relaxing factor released from the vascular endothelium.

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