Role of Norepinephrine and 5-Hydroxytryptamine in the Delayed Phase of the Inflammatory Reaction in Rats

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Abstract
Two to 4 hr. after intradermal injection of 1 [mu]g norepinephrine, 20 [mu]g histamine provoked an enormous vascular response, 2 to 3 times the extent and intensity of the response obtained in saline-treated rats. In rats depleted with 48/80 [p-methoxyphenethyl-methylamine condensation product with formaldehyde] or Polymixin-B, histamine failed to produce increased capillary permeability, but when 1ug norepinephrine was injected intradermally, histamine provoked a strong vascular permeability when injected 2 to 4 hr. later into the same site. In rats pretreated with reserpine, histamine or 5-hydroxytryptamine, 48/80 or Polymixin-B did not induce increased capillary permeability. The delayed vascular response did not occur after intradermal injection of norepinephrine, when challenged 2 to 4 hr. later with histamine, 48/80, or Polymixin-B, but increased permeability appeared when 5-hydroxytryptamine was injected. The delayed vascular response provoked by histamine 2 to 4 hr. after norepinephrine pretreatment was partially inhibited by chlorpromazine, levomepromazine and promethazine. LSD [lysergic acid diethylamide] aggravated the same delayed vascular response. The 3 inflammatory mediators of mast cell origin cooperate in the delayed inflammatory vascular response.

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