Adrenergic modulation of‘non‐adrenergic’twitches in the rat vas deferens

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Abstract
1 Field stimulation of the intramural sympathetic nerves of rat vas deferens produced a biphasic contraction. Post-tetanic twitches were potentiated (PTP) and the relationship of this to the secondary component of tetanic responses was investigated. 2 A tetanus evoked by field stimulation at 4 Hz for 50 s gave a maximum increase in twitch tension of 109 .+-. 5% (n = 43). The potentiation was blocked by the .alpha.-adrenoreceptor antagonists phenoxybenzamine, prazosin and thymoxamine. These drugs also blocked the secondary component of the tetanic response. 3 Increasing the frequency (1-8 Hz) of tetanic field stimulation enhanced the magnitude and time course of PTP. The time course of the PTP was found to depend mainly on the number of pulses in the tetanic train. 4 Reducing transmitter release in high Mg2+ solutions shortened the duration of the PTP but prevented the decline of the secondary tetanic component. Co2+ (1 mM) or Mn2+ (1 mM) mimicked the effect of high Mg2+ ions on the secondary tetanic component. Enhanced transmitter release in zero Mg2+-Krebs had the reverse effects. 5 The presynaptic .alpha.2-adrenoreceptor antagonists idazoxan and yohimbine, and the neuronal uptake blockers desipramine and metaraminol, prolonged the PTP and enhanced but shortened the secondary rise in tetanic tension. 6 Bolus injections of noradrenaline before and after the tetanus gave no evidence for post-synaptic desensitization. 7 It is concluded that both the secondary rise in tetanic tension and the posttetanic potentiation are due to an adrenergic enhancement of the ''non-adrenergic'' mechanism and not, as has been supposed, to direct activation of an adrenergic tension. Thus the action of the .alpha.-adrenoreceptor-mediated transmission is primarily one of modulation.