ACTIVATION of α adrenoceptors on noradrenergic nerve endings is thought to inhibit the release of noradrenaline by nerve impulses1,2. The existence of a presynaptic receptor system introduces a new concept to the pharmacology of drugs with affinity for α adrenoceptors. Only when the presynaptic nerve does not secrete, as for example in the absence of impulses, may one assume a priori that the observed postsynaptic effects of these drugs result from their interaction with postsynaptic receptors. When action potentials arrive at the nerve endings, noradrenaline is released and keeps the postsynaptic receptors in a certain degree of excitation. Drugs which activate α adrenoceptors may enhance this excitation by their postsynaptic effects, or reduce it by their presynaptic actions. Conversely, α adrenolytic drugs may diminish the excitation by postsynaptic blockade, or enhance it by facilitation of release. If the postsynaptic receptors are of the β type, the prevailing action is presynaptic; thus, drugs which activate a adrenoceptors reduce3–5, whereas, less regularly, α adrenolytic drugs increase6 cardiac responses to sympathetic nerve stimulation. If the postsynaptic receptors are of the α type, the prevailing effect of a adrenolytic drugs is postsynaptic blockade7; we report here that the effects of drugs which activate α adrenoceptors are diverse.
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