In segments of rabbit basilar artery (BA) platelet-activating factor (PAF) initiated a concentration-dependent transitory contraction which was unaffected by indomethacin or nordihydroguaiaretic acid (NDGA). Nω-nitro-L-arginine (NLA) did not change the magnitude of PAF-induced contraction, but in the presence of NLA the contraction tended to be more prolonged. In precontracted BA segments, PAF caused a concentration-dependent relaxation which was unaffected by NDGA. Indomethacin and NLA decreased PAF-induced relaxation by 10-30 and 70-90%, respectively; in combination these agents totally eliminated PAF-induced vessel reactions. Treatment of BA segments by rabbit peritoneal polymorphonuclear leukocytes (PMNLs) activated with N-formyl-methionyl-leucyl-phenylalanine (fMLP) for 20 min led to PMNL adhesion to the vascular endothelium and a significant decrease (60-100%) in acetylcholine-induced endothelium-dependent vessel relaxation. After the treatment of BA segments, PAF induced strong, slow, tonic contraction of either non-precontracted or precontracted vessels which was unaffected by indomethacin or NLA. NDGA decreased this contraction by 30-60%. These results indicate that PAF is an endothelium-dependent vasodilator that can also produce an insignificant constrictor effect. However, when the vessels are affected by activated PMNLs, PAF is transformed to a strong vasoconstrictor, presumably due to the generation of as yet unknown vasoconstrictor stimuli resulting from PMNL-endothelium interactions. Under these conditions the PAF-induced contraction is partly mediated by 5-lipoxygenase metabolites