Abstract
The activity of the sympathetic nervous system can be modulated by a variety of endogenous and exogenous substances which act at specific receptors located either at the postganglionic sympathetic nerve terminals or at the ganglia. Several investigators have reported that varicosities of postganglionic sympathetic nerves contain specific receptors, referred to as presynaptic receptors, activation of which leads to either inhibition or facilitation of NA release during sympathetic nerve stimulation (Lokhandwala, 1979b; Langer, 1980; Lokhandwala and Eikenburg, 1983; Starke, 1987). The presence of a negative feedback presynaptic alpha-adrenoceptor mechanism involved in modulating NA release is now well recognised (Langer, 1980; Starke, 1987). It is reported that NA released from sympathetic nerves activates presynaptic alpha-2-adrenoceptors, inhibits further transmitter release and, hence, controls its own release and subsequently its concentration within the synaptic cleft. Experimental evidence provided in support of this hypothesis is that blockade of presynaptic alpha-2-adrenoceptors and the removal of the endogenous NA on these receptors results in a greater release of the transmitter during sympathetic nerve stimulation and a potentiation of the effector response (Lokhandwala and Buckley, 1976; Langer et al., 1977; Starke, 1987).
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© 1988 Mustafa F. Lokhandwala and Maria Laura DeFeo
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Lokhandwala, M.F., DeFeo, M.L. (1988). Neuronal Dopamine Receptors. In: Bell, C., McGrath, B. (eds) Peripheral Actions of Dopamine. Satellite Symposia of the IUPHAR 10th International Congress of Pharmacology. Palgrave, London. https://doi.org/10.1007/978-1-349-09503-2_10
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