Increased platelet calcium in thrombosis and related disorders and its correction by nifedipine.
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.
D001161:Arteriosclerosis / Q000097:blood / Q000188:drug therapy; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000097:blood*; D006706:Homeostasis; D006801:Humans; D009543:Nifedipine / Q000494:pharmacology*; D013927:Thrombosis / Q000097:blood* / Q000188:drug therapy; D014652:Vascular Diseases / Q000097:blood / Q000188:drug therapy
D009543:Nifedipine; D002118:Calcium