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Calcium‐dependent contractile response of arterial smooth muscle to a jellyfish toxin (pCrTX: Carybdea rastonii )
Author(s) -
Azuma Hiroshi,
Ishikawa Masayuki,
Nakajima Terumi,
Satoh Akihiko,
Sekizaki Satomi
Publication year - 1986
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.1476-5381.1986.tb10235.x
Subject(s) - phentolamine , guanethidine , bretylium , verapamil , chemistry , tetrodotoxin , medicine , vasoconstriction , endocrinology , postsynaptic potential , contraction (grammar) , calcium , tyramine , stimulation , pharmacology , adrenergic , biology , receptor
1 The purpose of the present experiments was to investigate the pharmacological mechanisms of the vasoconstriction caused by the toxin (pCrTX) which had been partially purified from the tentacles of the jellyfish Carybdea rastonii (‘Andonkurage’). 2 pCrTX (0.1 to 10 μg ml −1 ) produced a tonic contraction of rabbit aortic strips, which was nearly abolished in Ca 2+ ‐free medium and was significantly reduced by verapamil or diltiazem. 3 pCrTX stimulated 45 Ca 2+ ‐influx and this effect was markedly attenuated by verapamil. 4 pCrTX‐induced vasoconstriction was significantly attenuated by phentolamine, 6‐hydroxydopamine (6‐OHDA) and in low Na + ‐medium, but not by bretylium, guanethidine, reserpinization or tetrodotoxin (TTX). 5 pCrTX continuously and significantly increased the 3 H‐efflux from [ 3 H]‐noradrenaline preloaded aortic strips and this effect was completely inhibited by pretreatment with 6‐OHDA and in Ca 2+ ‐free medium, but not by phentolamine, bretylium, guanethidine or TTX. 6 A single exposure to pCrTX for 30 min greatly reduced the contractile responses to tyramine, nicotine and transmural electrical stimulation, but not those to noradrenaline or KCl. In addition, incorporation of [ 3 H]‐noradrenaline was reduced. 7 Pretreatments with chlorphenylamine or indomethacin failed to modify the contractile response to pCrTX. 8 These results suggest that the pCrTX‐induced vasoconstriction is caused by a presynaptic action, releasing noradrenaline from the intramural adrenergic nerve terminals, and by a postsynaptic action, which consists at least in part of stimulation of the transmembrane calcium influx. Both pre‐ and postsynaptic actions depend on the external calcium concentration. The data further suggest that pCrTX damages the noradrenaline uptake and/or storage mechanisms without damaging postsynaptic contractile systems.