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Updated: Oct 1, 2026

Measuring Fast Calcium Fluxes in Cardiomyocytes
Published on: November 29, 2011
Effect of platelet release products on cytosolic calcium in cardiac myocytes
W W Chien1, R Mohabir, D Newman
1Division of Cardiology, Stanford University School of Medicine, CA 94305.
Insights
Activated platelets release heat-sensitive peptides that increase calcium in heart cells. These findings reveal a novel mechanism by which platelet products influence cardiac cell function.
Area of Science:
- Cardiovascular Biology
- Cell Physiology
- Platelet Biology
Background:
- Platelets play a crucial role in hemostasis and thrombosis.
- Platelet activation leads to the release of various bioactive substances.
- The impact of platelet release products on cardiac cell calcium regulation is not fully understood.
Purpose of the Study:
- To investigate the effect of platelet release products on cytosolic calcium levels in cardiac cells.
- To identify the nature of the platelet-derived factor responsible for altering calcium homeostasis.
Main Methods:
- Chick embryonic heart cells were loaded with the calcium indicator indo-1 AM.
- Cell-free filtrate from thrombin- or collagen-activated rabbit platelets was applied.
- Changes in cytosolic calcium concentration ([Ca++]i) were monitored via fluorescence.
- Characterization of the active substance involved heat, trypsin, molecular weight, and chemical sensitivity assays.
Main Results:
- Platelet release products induced a rapid, dose-dependent increase in both systolic and diastolic [Ca++]i.
- The effect was independent of thromboxane pathways and known platelet mediators like ADP and serotonin.
- The active component was a heat-sensitive, trypsin-sensitive peptide with a low molecular weight (<3 kD) and sensitivity to 2-mercaptoethanol.
Conclusions:
- Activated platelets release trypsin-sensitive peptides that elevate cytosolic calcium in cardiac cells.
- These peptides represent a novel class of platelet-derived mediators affecting cardiac function.
- Further research is warranted to elucidate the precise molecular identity and physiological relevance of these peptides.
Abstract:
The effect of platelet release products on cytosolic calcium [( Ca++]i) was examined by monitoring the fluorescence of chick embryonic heart cells loaded with the fluorescent calcium indicator indo-1 AM. Cell free filtrate of platelet release products was obtained from rabbit platelets activated with thrombin or collagen. This filtrate caused a rapid increase in both systolic and diastolic [Ca++]i in a dose-dependent manner. The effect was not blocked by pretreating the platelets with aspirin or a thromboxane synthetase inhibitor. It was not mimicked by a thromboxane analog, or by several substances known to be released from platelets including ADP, serotonin, or platelet activating factor. Apyrase or ATP-gamma S had no effect on the activity. The responsible product was heat-sensitive, trypsin-sensitive, and partitioned into the aqueous phase of a chloroform suspension. It has a low molecular weight (less than 3kD) and is sensitive to 2-mercaptoethanol. Protease inhibitor appears to prolong the activity. These results suggest that trypsin-sensitive peptide(s) released from activated platelets can increase [Ca++]i in cardiac cells.
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