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Calcium signalling in cardiac muscle cells
W G Wier1, J R López-López, P S Shacklock
1Department of Physiology, University of Maryland School of Medicine, Baltimore 21201, USA.
Ciba Foundation Symposium
|January 1, 1995
Summary
Heart cells exhibit distinct calcium ion (Ca2+) patterns, including waves, sparks, and controlled transients during excitation-contraction coupling. This study explores how Ca2+-induced Ca2+ release mechanisms generate these varied Ca2+ signals.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Biophysics
Background:
- Heart cells display diverse spatial patterns of cytoplasmic calcium ion concentration ([Ca2+]i).
- These include propagating [Ca2+]i waves, localized Ca2+ sparks, and evoked [Ca2+]i transients linked to excitation-contraction coupling.
- All transient types involve calcium-induced calcium release from the sarcoplasmic reticulum.
Purpose of the Study:
- To investigate how the autocatalytic process of calcium-induced calcium release generates controlled and uncontrolled [Ca2+]i signals in heart cells.
- To understand the mechanisms behind propagating [Ca2+]i waves, non-propagating Ca2+ sparks, and normal evoked [Ca2+]i transients.
- To explore the 'gain' of calcium-induced calcium release in cardiac function.
Main Methods:
- Confocal imaging of [Ca2+]i in heart cells.
- Analysis of spontaneous and evoked [Ca2+]i transients.
- Modeling of Ca2+ microdomains and release channel clusters.
Main Results:
- Evoked [Ca2+]i transients are controlled by L-type Ca2+ channel current.
- Calcium-induced calcium release underlies both spontaneous and controlled [Ca2+]i signals.
- A model involving Ca2+ microdomains and sarcoplasmic reticulum release channel clusters may explain signal diversity.
Conclusions:
- The diverse spatial patterns of [Ca2+]i in heart cells arise from variations in the calcium-induced calcium release process.
- Understanding these mechanisms is crucial for comprehending normal excitation-contraction coupling and pathological Ca2+ signaling.
- A microdomain model provides a framework for how localized events can lead to cell-wide or localized Ca2+ signals.