title: Characterization of the aggregation responses of camel platelets.
abstract: BACKGROUND
  Despite evidence of active hemostasis, camel platelets barely respond to common aggregating agents at standard doses used for human platelet aggregation.
  
  
  OBJECTIVE
  The purpose of the study was to find out whether camel platelets can be activated by high doses or combinations of aggregation agonists, and to characterize the receptor that mediates the aggregation response to adenosine diphosphate (ADP), the most potent agonist for camel platelets known so far.
  
  
  METHODS
  Aggregation studies were performed with platelet-rich plasma (PRP) in response to multiple doses or combinations of ADP, epinephrine (EPN), collagen, and arachidonic acid (AA). Aggregation responses to ADP were performed before and after the addition of the ADP receptor (P2Y12) antagonist Clopidogrel.
  
  
  RESULTS
  Camel platelets responded to ADP at doses higher than the standard dose for human platelets, and to combinations of EPN and other agonists, while no aggregation was elicited with EPN or AA alone. Clopidogrel blocked the ADP-induced aggregation responses in a dose-dependent fashion in vitro.
  
  
  CONCLUSIONS
  Camel platelet aggregation can be activated by increasing the dose of some agonists such as ADP, but not AA or EPN. Irreversible aggregation of camel platelets could also be triggered by a combination of EPN and ADP, and collagen and AA. Inhibition with clopidogrel suggests that camel platelets express the ADP receptor, P2Y12. Understanding platelet function in camels will add to the understanding of platelet function in health and disease.
authors.affiliation: The Coagulation Research Laboratory, College of Medicine and King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia.
authors.forename: Abeer K
authors.initials: AK
authors.lastname: Al Ghumlas
authors.forename: Abdel Galil M Abdel
authors.initials: AG
authors.lastname: Gader
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology*; D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D002162:Camelus / Q000502:physiology*; D000077144:Clopidogrel; D003094:Collagen / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D015539:Platelet Activation / Q000187:drug effects*; D010974:Platelet Aggregation / Q000187:drug effects*; D010979:Platelet Function Tests / Q000662:veterinary; D058921:Purinergic P2Y Receptor Antagonists / Q000494:pharmacology; D018048:Receptors, Purinergic P2 / Q000187:drug effects; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D058921:Purinergic P2Y Receptor Antagonists; D018048:Receptors, Purinergic P2; D016718:Arachidonic Acid; D000244:Adenosine Diphosphate; D003094:Collagen; D000077144:Clopidogrel; D013988:Ticlopidine; D004837:Epinephrine
keywords: Camelids; P2Y12 receptor; hemostasis; platelet activation