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OtherCELLULAR AND MOLECULAR PHARMACOLOGY

Possible Mechanism of Palytoxin-Induced Ca++Mobilization in Porcine Coronary Artery

Kazuo Ishii, Kaoru M. Ito, Daisuke Uemura and Katsuaki Ito
Journal of Pharmacology and Experimental Therapeutics June 1997, 281 (3) 1077-1084;
Kazuo Ishii
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Kaoru M. Ito
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Daisuke Uemura
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Katsuaki Ito
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Abstract

We investigated the mechanisms involved in palytoxin (PTX)-induced cytosolic Ca++ ([Ca++]i) mobilization and contraction in porcine coronary arteries using a fluorescent Ca++ indicator fura-PE3. PTX (1 pM-10 nM) induced concentration-dependent and sustained increases in [Ca++]i and tension, both of which were partially inhibited by 10 μM verapamil or 1 μM nicardipine. In Ca++-free solution containing 1 mM EGTA, PTX did not increase [Ca++]i. In nominally Ca++-free solution (no EGTA), however, PTX increased [Ca++]i, which was presumed to be due to release of Ca++ from intracellular stores. PTX-induced rise in [Ca++]i was dependent on external Na+ because it did not increase [Ca++]i in Na+-free solutions containing verapamil. An increase in [Ca++]iin response to 65.4 mM KCl also involved a verapamil-resistant but external Na+-dependent component. After blockage of voltage-dependent Ca++ channels with verapamil, elevation of external K+ to 65.4 mM enhanced the responses of [Ca++]i and tension to PTX. PTX at 10 and 100 pM depolarized the membrane by 4.5 ± 0.8 and 18.6 ± 1.7 mV, respectively. Because PTX is known to increase membrane Na+permeability, our results suggest that an increase in cytosolic Na+ and the depolarization were primary events required for the PTX-induced Ca++ mobilization and that Ca++influxes through voltage-dependent Ca++ channels and Na+-Ca++ exchange and Ca++ release from Ca++ stores, which was triggered by increased Ca++ entry, were responsible for the PTX-induced increase in [Ca++]i.

Footnotes

  • Send reprint requests to: Dr. Katsuaki Ito, Department of Veterinary Pharmacology, Faculty of Agriculture, Miyazaki University, Miyazaki 889-21, Japan.

  • Abbreviations:
    PTX
    palytoxin
    [Ca++]
    cytosolic Ca++ concentration
    [Na+]
    cytosolic Na+ concentration
    PSS
    physiological saline solution
    R340/380
    the ratio of fluorescence at emission of 500 nm after excitation at wavelength of 340 nm to that after excitation of 380 nm
    NMDG
    N-methyl-d-glucamine
    EGTA
    ethyleneglycol bis(β-aminoehtyl ether)-N,N′-tetraacetic acid
    SR
    sarcoplasmic reticulum
    • Received November 11, 1996.
    • Accepted February 24, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 281, Issue 3
1 Jun 1997
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Possible Mechanism of Palytoxin-Induced Ca++Mobilization in Porcine Coronary Artery

Kazuo Ishii, Kaoru M. Ito, Daisuke Uemura and Katsuaki Ito
Journal of Pharmacology and Experimental Therapeutics June 1, 1997, 281 (3) 1077-1084;

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OtherCELLULAR AND MOLECULAR PHARMACOLOGY

Possible Mechanism of Palytoxin-Induced Ca++Mobilization in Porcine Coronary Artery

Kazuo Ishii, Kaoru M. Ito, Daisuke Uemura and Katsuaki Ito
Journal of Pharmacology and Experimental Therapeutics June 1, 1997, 281 (3) 1077-1084;
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