Abstract：
:Palytoxin induced increases in cytosolic Ca2+ and tension, which were dependent on external Ca2+, and depolarized the membrane in endothelium-denuded porcine coronary arteries. When the endothelium was present, however, these effects were greatly inhibited, suggesting that some factors from endothelium inhibited the palytoxin-actions. Pretreatment with 100 microM N omega-nitro-L-arginine partially reversed the inhibitory effect of endothelium on the Ca2+ movement and the contraction but not that on the depolarization. Pretreatment with 10 microM indomethacin did not affect the inhibition. These results suggest that palytoxin released both nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) from the endothelium, both of which counteracted the actions of palytoxin on smooth muscle cells. It is thought that the palytoxin-induced depolarization was attenuated by hyperpolarization due to EDHF.
journal_name
Life Scijournal_title
Life sciencesauthors
Ishii K,Ito KM,Ikeda M,Uemura D,Ito Kdoi
10.1016/s0024-3205(96)00682-0subject
Has Abstractpub_date
1997-01-01 00:00:00pages
PL91-7issue
7eissn
0024-3205issn
1879-0631pii
S0024320596006820journal_volume
60pub_type
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