Abstract
The documentation for the observation that depolarization-evoked adrenergic transmitter release from sympathetic neurones is decreased by α2-adrenoceptor agonists, while it is enhanced by α2-adrenoceptor antagonists seems overwhelming (Langer 1977, 1981; Starke 1977, 1981; Westfall 1977; Gillespie 1980; Vizi 1979). This has led to the autoreceptor theory, according to which noradrenaline release from sympathetic neurones is modulated by the neurogenic transmitter itself: activation of presynaptic α2-adrenoceptors initiates a negative feedback system which results in subsequent inhibition of transmitter release. Recently, this hypothesis has been challenged (Chan and Kalsner 1979; Kalsner 1979, 1980a, 1980b, 1981, 1982a, 1982b, 1983; Angus and Korner 1980; Angus et al. 1984).
Supported by P. Carl Petersen’s Fund and the Novo Foundation
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© 1986 Springer-Verlag Berlin Heidelberg
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Nedergaard, O.A. (1986). Presynaptic α-Adrenoceptor Control of Transmitter Release from Vascular Sympathetic Neurones in Vitro. In: Grobecker, H., Philippu, A., Starke, K. (eds) New Aspects of the Role of Adrenoceptors in the Cardiovascular System. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71313-2_3
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DOI: https://doi.org/10.1007/978-3-642-71313-2_3
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