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Agonist‐directed trafficking explaining the difference between response pattern of naratriptan and sumatriptan in rabbit common carotid artery
Author(s) -
Akin Demet,
Onaran H Ongun,
Gurdal Hakan
Publication year - 2002
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 - 10.1038/sj.bjp.0704710
Subject(s) - sumatriptan , agonist , rabbit (cipher) , medicine , anesthesia , carotid arteries , atropine , pharmacology , receptor , computer science , computer security
Sumatriptan or eletriptan produced vasocontraction in common carotid artery (CCA) by stimulating 5HT 1B receptors (see also Akin & Gurdal, this issue). Naratriptan as a 5HT 1B/D agonist, was unable to produce vasocontraction in this artery, but inhibited the vasocontractile response induced by sumatriptan or eletriptan. All these agonists inhibited forskolin‐stimulated cyclic AMP production with comparable potencies and maximal responses. This inhibition was mediated by 5HT 1B receptors: 5HT 1B antagonist SB216641 (1 μ M ) completeley antagonized sumatriptan‐, eletriptan‐ or naratriptan‐induced cyclic AMP inhibition, but 5HT 1D antagonist BRL15572 (1 μ M ) did not affect this response. Naratriptan‐induced stimulation of 5‐HT 1B receptors resulted only in adenylate cyclase inhibition, whereas stimulation of these receptors by sumatriptan or eletriptan produced vasocontraction as well. Hence, we concluded that the 5HT 1B ‐mediated inhibition of adenylate cyclase was not a sufficient condition to couple the receptor stimulation to vasocontraction. We discussed agonist‐induced trafficking as a plausible mechanism for the observed phenomenon.British Journal of Pharmacology (2002) 136 , 171–176; doi: 10.1038/sj.bjp.0704710