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Thapsigargin-induced [Ca2+]i increase activates sodium influx in human platelets
M Tepel1, H Wischniowski, W Zidek
1Medizinische Universitäts-Poliklinik, University of Münster, Germany.
Biochimica Et Biophysica Acta
|February 17, 1994
Summary
Elevated calcium levels in human platelets increase sodium concentration by promoting sodium influx. This suggests intracellular calcium stores regulate sodium permeability across the plasma membrane.
Area of Science:
- Biochemistry
- Cell Biology
- Physiology
Background:
- Cytosolic free calcium concentration ([Ca2+]i) plays a crucial role in platelet function.
- The relationship between intracellular calcium stores and sodium homeostasis in platelets is not fully understood.
Purpose of the Study:
- To investigate the effect of elevated [Ca2+]i on cytosolic free sodium concentration ([Na+]i) in human platelets.
- To elucidate the mechanism by which calcium influences sodium permeability.
Main Methods:
- Spectrofluorometric measurements of [Ca2+]i and [Na+]i in intact human platelets.
- Utilized fluorescent dyes sodium-binding-benzofuran-isophthalate and fura-2.
- Employed thapsigargin to inhibit endoplasmic Ca-ATPase and elevate [Ca2+]i.
Main Results:
- Thapsigargin significantly increased both [Ca2+]i and [Na+]i in platelets.
- The increase in [Na+]i occurred independently of extracellular calcium.
- Thapsigargin-induced [Na+]i increase was abolished without external sodium, indicating sodium influx.
- Thapsigargin-induced sodium influx was inhibited by NiCl2.
Conclusions:
- The filling state of intracellular calcium stores regulates plasma membrane permeability to sodium.
- Elevated [Ca2+]i promotes sodium influx into platelets.
- This finding provides insights into the interplay between calcium and sodium signaling in platelet physiology.