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Related Experiment Videos

Calcium release from aortic sarcoplasmic reticulum.

J Watras1, D Benevolensky, C Childs

  • 1Department of Medicine, University of Connecticut Health Center, Farmington 06032.

Journal of Molecular and Cellular Cardiology
|February 1, 1989
PubMed
Summary
This summary is machine-generated.

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Inositol 1,4,5-trisphosphate (IP3) triggers calcium release from canine aortic sarcoplasmic reticulum. This IP3-induced calcium release is slow and differs from other tissues, suggesting unique calcium channels.

Area of Science:

  • Cardiovascular Physiology
  • Cellular Biology
  • Molecular Pharmacology

Background:

  • Sarcoplasmic reticulum (SR) calcium release is crucial for muscle contraction.
  • Inositol 1,4,5-trisphosphate (IP3) is a known intracellular calcium-mobilizing second messenger.
  • The role of IP3 in vascular smooth muscle SR calcium release is not fully elucidated.

Purpose of the Study:

  • To investigate the ability of inositol 1,4,5-trisphosphate (IP3) to induce calcium release from canine aortic sarcoplasmic reticulum vesicles.
  • To characterize the properties of IP3-induced calcium release in this specific tissue.

Main Methods:

  • Utilized calcium indicators chlorotetracycline and antipyrylazo III to monitor calcium levels in isolated aortic SR vesicles.
  • Measured calcium accumulation in the presence of ATP and subsequent release upon IP3 addition.

Related Experiment Videos

  • Employed stopped-flow analyses to determine the kinetics of calcium release.
  • Investigated the effects of various ions (Mg2+, Ca2+) and agents (GTP[gamma-S], ruthenium red) on IP3-induced calcium release.

    • Main Results:

    • Canine aortic SR vesicles accumulated calcium with ATP and released approximately 25% upon addition of 7 microM IP3.
    • Inositol 2-phosphate, inositol 1,4-bisphosphate, and inositol 1,3,4,5-tetrakisphosphate did not induce calcium release.
    • IP3-induced calcium release was inhibited by Mg2+ and Ca2+, and unaffected by ruthenium red.
    • The release kinetics were significantly slower than caffeine-induced release in skeletal muscle SR and exhibited a biphasic pattern.

    Conclusions:

    • Inositol 1,4,5-trisphosphate (IP3) is capable of inducing calcium release from canine aortic sarcoplasmic reticulum.
    • The characteristics of aortic IP3-induced calcium release differ from those observed in platelets and skeletal muscle, particularly regarding ion sensitivity and kinetics.
    • The biphasic nature of the release suggests heterogeneity in the calcium release channels within the aortic SR.