SEPARATION OF PUTATIVE ALPHA-1A-ADRENOCEPTOR AND ALPHA-1B-ADRENOCEPTOR MEDIATED COMPONENTS IN THE TENSION RESPONSE OF THE RAT VAS-DEFERENS TO ELECTRICAL-FIELD STIMULATION

1 The effects of the putative alpha-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 x 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 ( < 2s) and a plateau ( > 4s) phase. We deduce from our pharmacological analysis that the early phase contains a putative alpha-1B-adrenoceptor component (susceptible to CEC or prazosin but not to nifedipine) and a P2-purinoceptor component (susceptible to suramin or nifedipine) whereas the plateau phase contains an alpha-1A-adrenoceptor component (susceptible to prazosin or nifedipine but not to CEC) and a P2-purinoceptor component (susceptible to suramin or nifedipine). 4 We suggest that the putative alpha-1B-adrenoceptors may be functionally confined to the synaptic region whereas the putative alpha-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 alpha-1A-adrenoceptors.