RESPONSES TO NORADRENALINE IN HUMAN SUBCUTANEOUS RESISTANCE ARTERIES ARE MEDIATED BY BOTH ALPHA-1-ADRENOCEPTORS AND ALPHA-2-ADRENOCEPTORS

In vitro experiments in a microvascular myograph were designed to characterize postjunctional α-adrenoceptors of human subcutaneous resistance arteries (normalised internal diameter 143-313 μm). Both the α1-selective agonist phenylephrine in the presence of 0.3 μM yohimbine and the α2-selective agonist B-HT 933 in the presence of 0.3 μM prazosin elicited prominent and concentration-dependent contractions. The maximum response to phenylephrine and B-HT 933 was not different from the response to high K physiological salt solution (125 mM K+), and the pD2 values (-log EC50) were 5.90 and 6.11, respectively. In the presence of the α2-selective antagonist yohimbine (0.3 μM), the α1-selective antagonist prazosin competitively antagonised the responses to phenylephrine; the pA2 of prazosin for the receptor which mediated the response to phenylephrine was 8.41. Blockade of either α2-adrenoceptors with 0.1 μM yohimbine or α1-adrenoceptors with 0.1 μM prazosin caused shifts to the right of the noradrenaline concentration-response curves and the shifts in pD2 were 0.69 and 0.61, respectively. The combination of the two antagonists at the above-mentioned concentrations caused a marked, parallel shift to the right of the noradrenaline concentration-response curve, the shift of the pD2 was 2.68. These results suggest that activation of both α1- and α2-adrenoceptors produces contractions in human subcutaneous resistance arteries, and that responses to noradrenaline in these vessels are mediated by both α-adrenoceptor subtypes.