There is increasing evidence that re-uptake into sympathetic nerve endings is the primary mechanism of noradrenaline inactivation, whereas enzymic degradation seems to be of minor importance for the termination of the action of neurally liberated noradrenaline on the effector organ (for references see Thoenen, Hiirlimann & Haefely, 1964a). The intensity and duration of the response of the effector organ is related to the concentration and duration of transmitter in the neighbourhood of the receptors and will therefore depend not only on the amount of noradrenaline liberated by the nerves but also on the extent of re-uptake into these nerves. Diffusion from the site of liberation and subsequent removal by the blood stream are also of importance in the removal of transmitter (Hertting & Schiefthaler, 1963; Thoenen, Hurlimann & Haefely, 1963a).The main purpose of the present investigation was to study the dependence of transmitter release on the rate of sympathetic-nerve stimulation. For this purpose it was necessary to eliminate the chief mechanism of inactivation of neurally released noradrenaline, re-uptake into sympathetic nerve endings. The results obtained also allow some conclusions to be drawn on the physiological importance of this process of uptake.The isolated perfused spleen of the cat seemed to offer favourable experimental conditions for the study of this problem. The splenic nerves of the isolated cat's spleen were stimulated repetitively at different frequencies. In order to keep the circulation within the organ constant at all rates of stimulation the effect of splenic nerve stimulation on vascular and trabecular smooth muscles was blocked by the a-adrenergic blocking agent, phenoxybenzamine. Re-uptake of liberated noradrenaline by the sympathetic nerve endings was blocked by giving cocaine and phenoxybenzamine. The noradrenaline content of the venous effluent, determined by bio-assay,

The effects of progressive anoxia on the hemodynamic changes in the pulmonary circuit were reinvestigated in anesthetized dogs. Evidence is presented that some increase in pulmonary arterial resistance takes place, but that the augmented output of the right ventricle is dominantly responsible for elevation of the pulmonary arterial pressure when anoxia affects the bodv as a whole.

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