We have previously suggested that differences in α-adrenoceptor-mediated responses of human digital arteries and metacarpal veins cannot be completely reconciled with mixed populations of postsynaptic α1- and α2-adrenoceptors in these tissues [1, 2].

These suggestions were based on the following observations: (a) the Arunlakshana and Schild plots constructed on the basis of antagonism of either phenylephrine or noradrenaline by yohimbine had slopes which were less than unity, thus confirming that the receptors could not be a homogeneous population; (b) prazosin reduced the maximal responses to noradrenaline in both veins and arteries, but to a greater extent in the former than in the latter; (c) pD2 values for the α1-adrenoceptor agonists methoxamine and phenylephrine, and for the α2-adrenoceptor agonists clonidine and oxymetazoline, were the same in arteries and veins, whereas pD2 values for noradrenaline and adrenaline were significantly higher in veins than in arteries; (d) the difference between the arteries and veins in their pD2 values for noradrenaline was maintained in the presence of neuronal and extraneuronal uptake blockade and α-adrenoceptor blockade, thus suggesting it was due to differences in the α-adrenoceptors themselves rather than reflecting differences in populations of other receptors or of neurotransmitter uptake mechanisms [3].

The second of these observations would suggest that if there was a mixed population of typical α1- and α2-adrenoceptors in the arteries and veins the proportion of prazosin-resistant (α2-) receptors was greater in arteries than in veins. This conclusion, however, was not compatible with the observation of the greater sensitivity of veins than arteries to noradrenaline, but not phenylephrine or methoxamine, which would indicate a greater proportion of α2-adrenoceptors in veins than in arteries.

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