Evidence for prazosin‐resistant, rauwolscine‐sensitive α‐adrenoceptors mediating contractions in the isolated vascular bed of the rat tail

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Abstract
1 The postjunctional α-adrenoceptors mediating contractions in the isolated vascular bed of the perfused rat tail have been investigated, in the presence and absence of an increase in perfusion pressure by arginine vasopressin (AVP). 2 In the absence of AVP, bolus doses of noradrenaline (NA) and phenylephrine produced pressor responses of similar time course, while UK-14,304 was practically inactive. Responses to noradrenaline were inhibited more by 0.05 μm prazosin than by 1 μm rauwolscine, suggesting the presence of α1-adrenoceptors. 3 Following a sustained elevation in perfusion pressure by AVP, both UK-14,304 and NA (the latter in the presence of 0.05 μm prazosin to inhibit α1-adrenoceptors) elicited dose-dependent pressor responses. The maximum response to UK-14,304 under these conditions was approximately 30% of the maximum response to NA in the absence of prazosin and AVP. Responses to phenylephrine were not affected by the AVP-induced increase in vascular tone. 4 In the presence of AVP, pressor responses to UK-14,304 were resistant to 0.05 μm prazosin and susceptible to antagonism by 1 μm rauwolscine (-log Kb 7.65 ± 0.15). Similarly, responses to NA in the presence of 0.05 μm prazosin and AVP were inhibited by 1 μm rauwolscine. This represents the first demonstration of prazosin-resistant, rauwolscine-sensitive α2-adrenoceptor-mediated responses in the vasculature of the rat tail. 5 These results suggest that in isolated vascular preparations, functional populations of postjunctional α2-adrenoceptors may be ‘uncovered’ by the presence of AVP.

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