Calcium release from aortic sarcoplasmic reticulum

J. Watras, D. Benevolensky, C. Childs

    Research output: Contribution to journalArticlepeer-review

    Abstract

    The ability of inositol 1,4,5-trisphosphate (IP3) and other inositol phosphates to induce calcium release from canine aortic sarcoplasmic reticulum vesicles was examined. Using the calcium indicator chlorotetracycline or antipyrylazo III, aortic vesicles were shown to accumulate calcium in the presence of ATP, and then release ~25% of the intravesicular calcium upon addition of 7 μM IP3. Inositol 2-phosphate, inositol 1,4-bisphosphate, and inositol 1,3,4,5-tetrakisphosphate did not induce calcium release from these vesicles, and GTP[γ-S] did not affect the IP3-induced calcium release. Aortic IP3-induced calcium release was not affected by ruthenium red, but was inhibited by Mg2+ and Ca2+, and thus differs from the Mg2+-insensitive IP3-induced calcium release in platelets and the ruthenium red-sensitive IP3-induced calcium pathway in skeletal muscle sarcoplasmic reticulum. Stopped-flow analyses showed that aortic IP3-induced calcium release was much slower than the caffeine-induced calcium release from skeletal muscle sarcoplasmic reticulum. Moreover, the aortic IP3-induced calcium release was biphasic, suggestive of heterogeneity of the putative calcium channels.
    Original languageEnglish
    Pages (from-to)125-130
    Number of pages5
    JournalJournal of molecular and cellular cardiology
    Volume21
    Issue number1
    Publication statusPublished - 1989

    Keywords

    • Animals
    • drug effects: Aorta
    • metabolism: Calcium
    • drug effects: Calcium Channels
    • Dogs
    • Inositol 1,4,5-Trisphosphate
    • pharmacology: Inositol Phosphates
    • Kinetics
    • drug effects: Sarcoplasmic Reticulum

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