THE EFFECT OF SYMPATHETIC NERVE STIMULATION IN CATS PRETREATED WITH A-METHYL-META-TYROSINE.
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Biomedical subjects
Publications and source records attributed to H THOENEN.
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Results are reported of a quantitative study of the potentiating effect of cocaine on the responses of the cat nictitating membrane to intravenously and intra-arterially injected noradrenaline, as well as to different types of sympathetic nerve stimulation. Responses of the membrane to noradrenaline were potentiated more with intravenous than with close-arterial injections. From studies of the responses of the nictitating membrane to various forms of sympathetic nerve stimulation before and after injection of cocaine, conclusions are drawn as to the extent to which the transmitter amine liberated by nerve activity is normally removed and its effect thereby limited in duration and extent. This uptake was greatest at low stimulus frequencies. The mechanism by which cocaine potentiates sympathetic responses is discussed.
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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 amines 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.
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