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Increased platelet calcium in thrombosis and related disorders and its correction by nifedipine
Insights
Platelet calcium levels are elevated in many disorders, except uremia. Nifedipine normalized these levels, suggesting calcium channel blockers may prevent thrombosis and atherosclerosis.
Area of Science:
- Biochemistry
- Hematology
- Pharmacology
Background:
- Platelets play a critical role in various thrombotic and vascular disorders.
- Disruptions in calcium homeostasis are implicated in platelet dysfunction.
Purpose of the Study:
- To investigate calcium homeostasis in platelets across diverse pathological conditions.
- To evaluate the effect of nifedipine on platelet calcium levels in these disorders.
Main Methods:
- Utilized chlorotetracycline (CTC) as a fluorescent probe to measure intracellular calcium levels.
- Assessed platelet calcium in healthy subjects and patients with thromboses, hypertension, diabetes mellitus, vasculitis, immune thrombocytopenia, thrombotic thrombocytopenic purpura, myelofibrosis, hemolytic anemias, and uremia.
Main Results:
- Significantly elevated platelet calcium levels were observed in all studied disorders except uremia.
- Nifedipine treatment reduced or normalized the elevated calcium levels in most patients.
- Discontinuation of nifedipine led to the recurrence of abnormal calcium levels.
Conclusions:
- Platelets in thrombotic disorders may experience enhanced calcium influx due to subcritical activating factors.
- Nifedipine protects platelets from these stimuli, indicating potential therapeutic benefits.
- Calcium channel blockers show promise as both antiatherogenic and antithrombotic agents.
Abstract:
Using chlorotetracycline (CTC) as a probe we studied calcium homeostasis of platelets in various disorders. Studied were healthy subjects and patients with disorders where platelets play an important role. These included thromboses, hypertension, diabetes mellitus, vasculitis, immune thrombocytopenia, thrombotic thrombocytopenic purpura, myelofibrosis, hemolytic anemias and uremia. Significant elevation of calcium levels were observed in all of these disorders except uremia. Nifedipine reduced or normalized the increased levels in most patients and its discontinuation resulted in a return of the abnormality. We propose that platelets in thromboses and related disorders are exposed to subcritical concentrations of activating factors, leading to enhanced calcium influx and elevated free cytoplasmic calcium followed by elevated resting dense tubular calcium. Nifedipine appears to protect platelets from these stimuli and coupled with their known action on vessel walls, calcium channel blockers show promise as antiatherogenic as well as antithrombotic agents.