Abstract
1 Noradrenaline (0.1-3.0 μM) inhibited the twitch responses to single pulse field stimulation of the isolated vas deferens of the mouse. The higher concentrations of noradrenaline (ca. 0.3-3.0 μM) were required to make the tissue contract.
2 Phentolamine (10 μM) abolished the contractor response to higher concentrations of noradrenaline and antagonized the inhibitory effect of lower concentrations on the twitch response.
3 Propranolol (10 μM) potentiated both the contractor and the inhibitory effect of noradrenaline on the twitch response.
4 Isoprenaline (0.1-3.0 μM) and salbutamol (1.0-3.0 μM) both inhibited the twitch response. Their effects were antagonized by propranolol (10 μM), but not by practolol (10 μM).
5 The effects of uptake1 and uptake2 blocking agents were determined. Cocaine (10 μM) reduced the size of the twitch response in 2 out of 4 experiments. Imipramine (0.18 μM) also reduced the size of the twitch, as did oestradiol (3.7 μM) and a combination of cocaine and oestradiol.
6 Contractor responses to exogenous noradrenaline showed tachyphylaxis, but when this was not very marked, the response could be shown to be potentiated by uptake blocking agents.
7 The inhibitory effect of noradrenaline on the twitch response was greatly potentiated by cocaine (10 μM) and much less so by oestradiol (3.7 μM).
8 It is concluded that the transmitter responsible for the twitch response is either an unknown substance released from the sympathetic neurone, or noradrenaline acting upon a receptor with none of the characteristics of known α- or β-adrenoceptors. In either case, noradrenaline can inhibit the output, probably by stimulation of presynaptic α-adrenoceptors.
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Selected References
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