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Capacitative Ca2+ entry in human platelets is resistant to nitric oxide
Y Okamoto1, H Ninomiya, S Miwa
1Department of Pharmacology, Faculty of Medicine, Kyoto University, Japan.
Biochemical and Biophysical Research Communications
|July 6, 1995
Summary
Sodium nitroprusside (SNP) and U73122 inhibit calcium influx in human platelets. However, nitric oxide does not affect capacitative calcium entry once triggered by inositol trisphosphate-induced store-depletion.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Thrombin stimulation of human platelets increases intracellular calcium (Ca2+).
- Calcium influx is crucial for platelet activation and function.
- The role of nitric oxide (NO) and phospholipase C (PLC) in regulating Ca2+ influx is not fully understood.
Purpose of the Study:
- To investigate the effect of sodium nitroprusside (SNP) and a phospholipase C inhibitor (U73122) on thrombin-induced Ca2+ influx in human platelets.
- To determine if nitric oxide affects capacitative Ca2+ entry in human platelets.
Main Methods:
- Human platelets were stimulated with thrombin (0.2 U/ml).
- Dose-dependent effects of SNP and U73122 on Ca2+ influx were measured.
- Capacitative Ca2+ entry was induced using thapsigargin and an acid extract from thrombin-stimulated platelets.
Main Results:
- Both SNP and U73122 inhibited thrombin-induced Ca2+ influx in a dose-dependent manner.
- A fraction of Ca2+ influx resistant to U73122 was also resistant to SNP, suggesting capacitative Ca2+ entry.
- SNP and U73122 did not inhibit Ca2+ influx induced by thapsigargin or a platelet-derived Ca2+ influx factor.
Conclusions:
- Capacitative Ca2+ entry in human platelets, triggered by inositol trisphosphate-induced store depletion, is not affected by nitric oxide.
- Nitric oxide and phospholipase C inhibition do not modulate the late phase of calcium influx in activated platelets.