title: Unstimulated polymorphonuclear neutrophils regulate proximal coronary arterial tone.
abstract: Our objective is to clarify, by measuring the superoxide production as a marker of inactive state of polymorphonuclear neutrophils, whether unstimulated polymorphonuclear neutrophils would influence coronary arterial tone. We recorded the isometric tension of the porcine coronary arterial ring in a bath of oxygenated Krebs Ringer solution. Unstimulated porcine polymorphonuclear neutrophils that contained little superoxide were added to the bath. We also analyzed the prostaglandins produced in the bath. The isometric tension of arterial rings increased dose-dependently when polymorphonuclear neutrophils were added to the bath. The vasoconstriction induced by unstimulated polymorphonuclear neutrophils was inhibited by endothelial denudation, indomethacin, anti-CD11a/18-like antibody. Thromboxane A2 synthetase inhibitor and superoxide dismutase did not effect the vasoconstriction. Prostaglandin E2 predominated among the prostaglandins produced in the bath; its production was significantly inhibited by indomethacin (without vs. with indomethacin; 3898 +/- 1704 vs 1956 +/- 715 pg/ml, P < 0.05, n=6). Pretreatment of vascular rings with indomethacin blocked the interaction of the coronary artery with polymorphonuclear neutrophils. Results suggested that unstimulated polymorphonuclear neutrophils constrict the proximal coronary artery. Such vasoconstriction may be produced by cyclooxygenase products, especially prostaglandin E2 produced in the vascular wall via the interaction between the polymorphonuclear neutrophils and the endothelium. Polymorphonuclear neutrophils may regulate coronary arterial tone.
authors.affiliation: First Department of Internal Medicine, Fukushima Medical College, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Abe
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: S
authors.initials: S
authors.lastname: Kuroda
authors.forename: T
authors.initials: T
authors.lastname: Ishibashi
authors.forename: M
authors.initials: M
authors.lastname: Keitoku
authors.forename: Y
authors.initials: Y
authors.lastname: Maruyama
mesh_terms: D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology; D015415:Biomarkers; D003331:Coronary Vessels / Q000502:physiology*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000502:physiology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007537:Isometric Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D011863:Radioimmunoassay; D013053:Spectrophotometry; D013481:Superoxides / Q000378:metabolism; D013552:Swine
chemical_list: D015415:Biomarkers; D016861:Cyclooxygenase Inhibitors; D013481:Superoxides; D016718:Arachidonic Acid; D015232:Dinoprostone; D007213:Indomethacin