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Neurally evoked responses of human isolated resistance arteries are mediated by both α m 1 ‐ and α 2 ‐adrenoceptors
Author(s) -
Parkinson N.A.,
Thorn S.McG.,
Hughes A.D.,
Sever P.S.,
Mulvany M.J.,
Nielsen H.
Publication year - 1992
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.1476-5381.1992.tb14376.x
Subject(s) - rauwolscine , prazosin , stimulation , antagonist , medicine , contraction (grammar) , endocrinology , chemistry , biology , receptor
1 Human subcutaneous resistance arteries (internal diameter 113–626 μ m ) were mounted in an isometric myograph. Electrical field stimulation was applied either continuously in the form of a frequency‐response curve or intermittently at 16 Hz. The magnitude of the maximum contraction induced by continuous stimulation expressed as a percentage of the response to a supramaximal concentration of noradrenaline (10 μ m ) was highly variable but unrelated to vessel calibre. Contractile responses to both continuous and intermittent stimulation were abolished by 1 μ m tetrodotoxin. 2 Prazosin (100 n m and 1 μ m , α 1 ‐adrenoceptor antagonist) inhibited responses to continuous stimulation over a range of frequencies (2–8 Hz). The response to continuous stimulation at 8 Hz was inhibited by 78 ± 6% by 1 μ m prazosin. Rauwolscine (100 n m , α 2 ‐adrenoceptor antagonist) had a smaller effect on contractions induced by continuous stimulation. Rauwolscine inhibited the response at 8 Hz by 36 ± 6%. Rauwolscine at a higher concentration (1 μ m ) caused further inhibition of the response to continuous stimulation. Prazosin and rauwolscine in combination almost completely inhibited the response to continuous stimulation at concentrations of 1 μ m . 3 Prazosin and rauwolscine inhibited responses to intermittent stimulation in a concentration‐dependent manner. The IC 50 for this action of prazosin was 3.7 ± 1.6 n m and the maximum inhibition induced by 100 n m prazosin was 78 ± 6%. The IC 50 of rauwolscine was 12.0 ± 1.3 n m and 100 n m rauwolscine caused a 86 ± 7% reduction in the response to intermittent stimulation. Prazosin and rauwolscine in combination (each at 100 n m ) caused marked inhibition of the response to intermittent stimulation leaving only 7.0 ± 2.6% of the response. 4 These data suggest that neurally released noradrenaline evokes contractions of human resistance arteries by activation of both α 1 and α 2 ‐adrenoceptors postjunctionally.

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