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Effects of reduced calcium ion concentration and of diltiazem on vasoconstrictor responses to noradrenaline and sympathetic nerve stimulation in rat isolated tail artery
Author(s) -
Medgett Iain C.,
Rajanayagam M. A. Sharmini
Publication year - 1984
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.1476-5381.1984.tb16528.x
Subject(s) - idazoxan , prazosin , diltiazem , stimulation , medicine , endocrinology , calcium , chemistry , extracellular , rauwolscine , antagonist , biology , receptor , biochemistry
1 In isolated, perfused proximal segments of Sprague‐Dawley rat tail artery, idazoxan (100 nmoll 1 ) displaced the concentration‐response curve to noradrenaline (NA) to the right. The log shift of the NA concentration‐response curve was greater at lower concentrations than at higher concentrations of NA. Idazoxan (100 nmoll −1 ) had no effect on responses to electrical stimulation. 2 Prazosin (10 nmoll −1 ) displaced the concentration‐response curve to NA to the right as well as markedly reducing responses to sympathetic nerve stimulation. 3 The concentration‐response curve to NA, obtained after reducing the concentration of calcium ions in the Krebs solution from 2.5 to 0.6 mmoll −1 , was significantly displaced to the right. Responses to sympathetic nerve stimulation were not affected by this reduction in the concentration of calcium ions. 4 Diltiazem (1 and 10 μmoll −1 ) significantly displaced the concentration‐response curve to NA to the right but had no effect on sympathetic nerve stimulation. 5 These in vitro results in peripheral arterial smooth muscle confirm the findings of previous in vivo studies which suggest that α 2 ‐adrenoceptors contribute to the vasoconstrictor responses elicited by α‐adrenoceptor agonists and that these responses but not those mediated by α 1 ‐adrenoceptors are dependent on extracellular calcium.