Abstract
The present study investigated the mechanisms by which the thromboxane A2 mimetic U46619 can elicit phasic and tonic contractions in the pig thoracic duct, whereas other agonists like 5-hydroxytryptamine (5-HT) produce tonic contractions only. Tonic contractions in response to either agonist were abolished by the l-type voltage-operated calcium channel (VOCC) inhibitor nifedipine, the store-operated calcium channel inhibitor SKF 96365, the calcium-sensitive chloride channel (ClCa) inhibitor niflumic acid, and by removal of extracellular Cl-. Superimposed phasic responses to U46619 were abolished by only nifedipine. Inhibitors of K+ channels did not prevent phasic contractions to U46619. The IP3 receptor antagonist 2-APB attenuated tonic contractions only, whereas ryanodine and removal of extracellular Na+ selectively abolished phasic contractions to U46619. Therefore, selective initiation of phasic contractions by U46619 appears to depend on intracellular Ca2+ from a ryanodine-sensitive store that causes depolarization via Na+/Ca2+ exchange, whereas tonic contractions to U46619 and 5-HT are mediated primarily by release of IP3-mobilized intracellular Ca2+ that subsequently causes ClCa opening, membrane depolarization, and Ca2+ entry via l-type VOCC.
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