The Responses to Tyramine of the Normal and Denervated Nictitating Membrane of the Cat: Analysis of the Mechanisms and Sites of Action

Abstract

The response to tyramine of the denervated nictitating membrane has been analysed by comparing dose/response curves obtained by injections into the femoral vein and into the carotid artery of the spinal cat while recording contractions of innervated and chronically denervated membranes and those of cats treated with reserpine. It is concluded that the effect of tyramine given by these routes is due primarily to catechol amines released from stores within the nictitating membrane itself. Higher doses of tyramine also cause contraction of the membrane by liberating catechol amines into the circulating blood from stores outside the membrane. The response to tyramine of the nictitating membrane after chronic denervation and/or prior treatment with reserpine is partially due to catechol amines released from unidentified stores within the membrane which resist depletion by reserpine and by postganglionic denervation; evidence is presented that adrenaline rather than noradrenaline is concerned. Because of the high sensitivity of the denervated nictitating membrane to adrenaline and to noradrenaline, the response to these a-mines released from stores outside the membrane by intravenous injections of tyramine becomes greater than that of the normal membrane. Dose/response curves obtained from responses to intravenous sympathomimetic drugs which act away from the membrane are therefore not fully representative of the effect of the drugs on the membrane itself. Tyramine probably has an affinity both for storage sites and for catechol amine receptors in the smooth muscle of the nictitating membrane, the "intrinsic activity," however, being very weak or even absent.It is generally accepted that tyramine owes at least the main part of its sympathomimetic effect to the release of the normal sympathetic transmitter from stores within or in the vicinity of adrenergic nerve endings. Experiments published in the last two years have supplied direct proof for such an effect in vivo as well as in

Pressor response to oral tyramine during co-administration with safinamide in healthy volunteers

“…Tyramine is an indirect sympathomimetic amine, producing its pharmacological effects almost exclusively by releasing noradrenaline from noradrenergic nerve terminals (Burn and Rand 1958;von Euler and Lishajko 1960;Axelrod et al 1962;Shuemann and Philippu 1962;Haefely et al 1963;Da Prada et al 1988). Endogenous tyramine is formed in various biosynthetic pathways and is one of the trace amines present in minute amounts in the central nervous system (Boulton and Dyck 1974;Baker et al 1982;Boulton 1978;Karoum 1983;Juorio et al 1985).…”