Separation of putative α 1A ‐ and α 1B ‐ adrenoceptor mediated components in the tension response of the rat vas deferens to electrical field stimulation

1 The effects of the putative α 1B ‐adrenoceptor antagonist, chloroethylclonidine (CEC), on tension responses of the rat isolated whole vas deferens to single and multiple pulses of electrical field stimulation have been evaluated by use of a microcomputer system which enables the averaging of like‐responses throughout their time course. 2 CEC (10 −7 to 3 × 10 −6 m ) selectively and in a concentration‐dependent manner blocked the noradrenergic component of the response to a single field stimulus in the absence or presence of nifedipine (10 −5 m , which blocked the purinergic but not the noradrenergic component of the response). The concentration‐response curve of the vas to exogenously‐applied noradrenaline (NA) was unaffected by CEC (10 −6 m ) but was flattened by nifedipine (10 −5 m ). 3 The tension response to 10 Hz trains of pulses was biphasic, with an early (< 2 s) and a plateau (> 4 s) phase. We deduce from our pharmacological analysis that the early phase contains a putative α 1B ‐adrenoceptor component (susceptible to CEC or prazosin but not to nifedipine) and a P 2 ‐purinoceptor component (susceptible to suramin or nifedipine) whereas the plateau phase contains an α 1A ‐adrenoceptor component (susceptible to prazosin or nifedipine but not to CEC) and a P 2 ‐purinoceptor component (susceptible to suramin or nifedipine). 4 We suggest that the putative α 1B ‐adrenoceptors may be functionally confined to the synaptic region whereas the putative α 1A ‐adrenoceptors are excluded from this region. Trains of pulses would allow NA to accumulate and spill out beyond the synaptic region to reach and activate the putative α 1A ‐adrenoceptors.