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Substance P As Neurogenic Mediator Of Antidromic Vasodilation And Neurogenic Plasma Extravasation

F. Lembeck, P. Holzer
Published 2004 · Chemistry, Medicine

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Summary1.Antidromic vasodilation and neurogenic plasma extravasation were induced by antidromic stimulation of the saphenous nerve in guanethidine-treated rats. Vasodilation was measured by the change of outflow from the femoral vein and plasma extravasation was determined by Evans blue exudation.2.Antidromic vasodilation was reduced by 85% in adult rats which were pretreated with capsaicin on the second day of life.3.Antidromic vasodilation was inhibited by 46% after pretreatment with cimetidine plus mepyramine and by 64% after pretreatment with compound 48/80, but was not affected by pretreatment with cimetidine, atropine, methysergide, or indomethacin. Similarly, neurogenic plasma extravasation was reduced by 50% after pretreatment with cimetidine plus mepyramine, and by 88% after pretreatment with compound 48/80, but was not altered after pretreatment with indomethacin.4.Infusion of substance P into the femoral artery dose-dependently produced vasodilation (threshold: 0.1 pmol min−1) and plasma extravasation (threshold: 0.5 pmol·min−1). Vasodilation induced by substance P was inhibited by 47% after pretreatment with cimetidine plus mepyramine and by 58% after pretreatment with compound 48/80. Plasma extravasation induced by substance P was reduced by 61% after pretreatment with cimetidine plus mepyramine and by 81% after pretreatment with compound 48/80. Pretreatment with indomethacin had no influence on substance P-induced vasodilation and plasma extravasation.5.It is concluded that vasodilation and plasma extravasation following antidromic stimulation of sensory nerves are initiated by peripheral release of substance P from chemosensitive pain fibres. The actions of substance P include, besides direct effects, release of histamine from mast cells.
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