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Responses to noradrenaline in human subcutaneous resistance arteries are mediated by both α 1 ‐ and α 2 ‐adrenoceptors
Author(s) -
Nielsen H.,
Mortensen F.V.,
Mulvany M.J.
Publication year - 1990
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1990.tb14649.x
Subject(s) - prazosin , yohimbine , phenylephrine , schild regression , agonist , endocrinology , medicine , myograph , antagonist , alpha (finance) , chemistry , pharmacology , receptor , vasodilation , blood pressure , construct validity , nursing , patient satisfaction
1 In vitro experiments in a microvascular myograph were designed to characterize postjunctional α‐adrenoceptors of human subcutaneous resistance arteries (normalised internal diameter 143–313 μ m ). 2 Both the α 1 ‐selective agonist phenylephrine in the presence of 0.3 μ m yohimbine and the α 2 ‐selective agonist B‐HT 933 in the presence of 0.3 μ m 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 m m K + ), and the pD 2 values (−log EC 50 ) were 5.90 and 6.11, respectively. 3 In the presence of the α 2 ‐selective antagonist yohimbine (0.3 μ m ), the α 1 ‐selective antagonist prazosin competitively antagonised the responses to phenylephrine; the pA 2 of prazosin for the receptor which mediated the response to phenylephrine was 8.41. 4 Blockade of either α 2 ‐adrenoceptors with 0.1 μ m yohimbine or α 1 ‐adrenoceptors with 0.1 μ m prazosin caused shifts to the right of the noradrenaline concentration‐response curves and the shifts in pD 2 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 pD 2 was 2.68. 5 These results suggest that activation of both α 1 ‐ and α 2 ‐adrenoceptors produces contractions in human subcutaneous resistance arteries, and that responses to noradrenaline in these vessels are mediated by both α‐adrenoceptor subtypes.