Vascular endothelium releases vasocontracting and/or vasorelaxing substances. Here, we report the diversity of endothelium-derived vasocontracting factors (EDCFs), arachidonic acid metabolites, and discuss the pathophysiological significance. In the canine basilar artery and the rabbit intrapulmonary artery, acetylcholine-induced contractions (ACh-induced EDC) are due to endothelial thromboxane A2 (TXA2) (TXA2-type). The ACh-induced EDC in the rabbit coronary artery is due to endothelial leukotrienes (LTs) (LTs-type). In addition, in the rat coronary artery, nicotine and noradrenaline (NAd)-induced EDCs are due to endothelial COX-metabolites (COX metabolite-type). These arachidonic acid metabolites derived from endothelium (activation by vasoactive substances including ACh, NAd and nicotine) cause a contraction of vascular smooth muscle cells and may disturb the local circulation. These EDCFs (TXA2, LTs and COX-metabolites) may be involved in the pathophysiology of cardiovascular immuno-inflammatory diseases.
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