Inositol 1,4,5-Trisphosphate But Not Ryanodine-Receptor Agonists Induces Calcium Release from Rat Liver Golgi Apparatus Membrane Vesicles

Inositol 1,4,5-Trisphosphate But Not Ryanodine-Receptor Agonists Induces Calcium Release from Rat... We investigated the direct effect of inositol 1,4,5-trisphosphate (IP3) and ryanodine receptor agonists on Ca2+ release from vesicles of a rat liver Golgi apparatus (GA) enriched fraction, which were actively loaded with 45Ca2+. Results in GA were compared with those obtained in a rat liver endoplasmic reticulum (ER) enriched fraction. The addition of IP3 at concentrations ranging from 100 nm to 100 μm, in the presence of thapsigargin, a specific inhibitor of sarcoplasmic/endoplasmic reticulum Ca2+-ATPases, promoted a rapid decrease in the Ca2+ content of GA vesicles. The amount of Ca2+ released from the vesicles was a function of IP3 concentration, reaching about 60% in both GA and ER fractions at 100 μm IP3. Calcium release was inhibited by heparin, an antagonist of IP3 receptors. Calcium exhibited a bell-shaped effect on IP3-dependent Ca2+ released from GA vesicles: it activated Ca2+ release at concentrations up to 1 μm, and inhibited it at higher concentrations. In contrast to that found in the endoplasmic reticulum fraction, none of the ryanodine receptor agonists tested (cyclic ADP-ribose, caffeine and ryanodine) significantly induced Ca2+ release from GA fraction vesicles in the presence of thapsigargin. Our results indicate the presence of an IP3-sensitive Ca2+ release mechanism in the Golgi apparatus membrane analogous to that of the ER. However, a Ca2+ release mechanism sensitive to ryanodine receptor agonists like that of ER is not evident in the GA membrane. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Inositol 1,4,5-Trisphosphate But Not Ryanodine-Receptor Agonists Induces Calcium Release from Rat Liver Golgi Apparatus Membrane Vesicles

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Publisher
Springer-Verlag
Copyright
Copyright © Inc. by 2000 Springer-Verlag New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s002320010008
Publisher site
See Article on Publisher Site

Abstract

We investigated the direct effect of inositol 1,4,5-trisphosphate (IP3) and ryanodine receptor agonists on Ca2+ release from vesicles of a rat liver Golgi apparatus (GA) enriched fraction, which were actively loaded with 45Ca2+. Results in GA were compared with those obtained in a rat liver endoplasmic reticulum (ER) enriched fraction. The addition of IP3 at concentrations ranging from 100 nm to 100 μm, in the presence of thapsigargin, a specific inhibitor of sarcoplasmic/endoplasmic reticulum Ca2+-ATPases, promoted a rapid decrease in the Ca2+ content of GA vesicles. The amount of Ca2+ released from the vesicles was a function of IP3 concentration, reaching about 60% in both GA and ER fractions at 100 μm IP3. Calcium release was inhibited by heparin, an antagonist of IP3 receptors. Calcium exhibited a bell-shaped effect on IP3-dependent Ca2+ released from GA vesicles: it activated Ca2+ release at concentrations up to 1 μm, and inhibited it at higher concentrations. In contrast to that found in the endoplasmic reticulum fraction, none of the ryanodine receptor agonists tested (cyclic ADP-ribose, caffeine and ryanodine) significantly induced Ca2+ release from GA fraction vesicles in the presence of thapsigargin. Our results indicate the presence of an IP3-sensitive Ca2+ release mechanism in the Golgi apparatus membrane analogous to that of the ER. However, a Ca2+ release mechanism sensitive to ryanodine receptor agonists like that of ER is not evident in the GA membrane.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Oct 1, 2000

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