1. In order to compare pre- and post-synaptic mechanisms influencing human vascular smooth muscle contraction, post-mortem digital arteries have been studied in vitro. After preloading transmitter stores with [3H]noradrenaline, stimulation-induced total tritium outflow and the associated pressure response were measured.

2. Tetrodotoxin either partially or completely abolished both stimulation-induced tritium outflow and constrictor response.

3. Neither the total tritium outflow nor the degree of its reduction by tetrodotoxin was related to the time after death the arteries were removed. Similarly no correlation was observed between stimulation-induced tritium outflow and age, sex, previous medications or underlying disease of the patient from whom the arteries were removed.

4. Total tritium outflow per impulse was markedly enhanced by increasing the frequency of stimulation from 1 Hz to 6 Hz.

5. Cocaine produced only a modest increase in stimulation-induced tritium outflow. Phentolamine more markedly enhanced stimulation-induced tritium outflow, whereas clonidine significantly reduced the outflow, thus demonstrating the presence of presynaptic α-adrenoreceptors.

6. It is concluded that post-mortem human digital arteries are suitable for the study of adrenergic transmitter release in man and that the two most important factors influencing transmitter release are frequency of stimulation and presynaptic receptors.

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