Sarafotoxin-induced calcium mobilization in cultured dog tracheal smooth muscle cells

Chuenchuen Mao Yang*, Richard Ong, Jen Tsung Hsieh, Ying Ling Yo

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

6 Scopus citations


Sarafotoxin b (S6b) -induced changes in intracellular Ca[2+] concentration ([Ca 2+]i) were monitored in cultured canine tracheal smooth muscle cells (TSMCs) by a fluorescent Ca2+ indicator fura-2. S6b elicited an initial transient peak followed by a sustained elevation of [Ca2+]i. BQ-123, an endothelin (ETA) eceptor antagonist, had a high affinity to block the rise [Ca2+]i response to S6b. In the absence of external Ca2+, only an initial transient peak of [Ca2+]i was seen, the sustained elevation of [Ca2+]i could then be evoked by addition of 1.8 mM [Ca2+] Ca2+ influx was required for the changes of [Ca2+]i, since the Ca2+-channel blockers, diltiazem, verapamil, an& Nip+ decreased both the initial and sustained elevation of [Ca2+Ii in response to S6b. TSMCs pretreated with phorbol 12-myristate 13- acetate (PMA, 1 (M) for 30 min attenuated Ca2+ mobilization induced by S6b, w ich was reversed by stauros orine, a protein kinase C (PKC) inhibitor. The change of [Ca2P] + induced by S6b was attenuated by cholera toxin pretreatmenk, but not by pertussis toxin. These data demonstrate that the initial detectable increase in [Ca2+Ii stimulated by S6b is due to the activation of ETA receptors and subsequent release of Ca2+ internal stores, whereas the contribution of external Ca2+ follows and partially involves a diltiazem- and verapamil-sensitive process. The inhibition of PMA on S6b-induced Ca2+ mobilization was inversely correlated with membraneous PKC activity.

Original languageEnglish
Pages (from-to)423-445
Number of pages23
JournalJournal of Receptors and Signal Transduction
Issue number6-8
StatePublished - 1994


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