Key result
Inositol 1,4,5-trisphosphate (IP3) up to 50 microM was ineffective in causing Ca2+ release from permeabilized cardiac myocytes and isolated canine cardiac sarcoplasmic reticulum vesicles.
Population
Saponin-permeabilized myocytes and isolated canine cardiac sarcoplasmic reticulum vesicles
Design
Preclinical
Authors
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Challenges IP3 as cardiac Ca2+ second messenger; leaves open its physiological relevance in intact models.
This preclinical study demonstrates that IP3 is unlikely to act as a Ca2+-mobilizing second messenger in cardiac muscle.
Movsesian et al. (1985) studied this question. Inositol 1,4,5-trisphosphate (IP3) was evaluated on Ca2+ release from intracellular stores. Inositol 1,4,5-trisphosphate (IP3) up to 50 microM was ineffective in causing Ca2+ release from permeabilized cardiac myocytes and isolated canine cardiac sarcoplasmic reticulum vesicles.
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