A surface NAD-glycohydrolase of human platelets may influence their aggregation.
Human platelets may hydrolyze externally added NAD+ yielding ADPR and nicotinamide. The extent of hydrolysis is significantly higher when the platelets are stimulated. The presence of external NAD+ strongly inhibits the aggregation induced by every agonist used. It seems that adenosine or ADPR itself generated by NAD+ hydrolysis may be responsible for the inhibition of aggregation. Evidence is given that some of the NAD+ hydrolysis product is taken up by stimulated platelets.
D000241:Adenosine / Q000494:pharmacology; D000246:Adenosine Diphosphate Ribose / Q000494:pharmacology; D001792:Blood Platelets / Q000201:enzymology*; D002462:Cell Membrane / Q000201:enzymology; D006801:Humans; D009243:NAD / Q000494:pharmacology; D009244:NAD+ Nucleosidase / Q000097:blood* / Q000502:physiology; D009536:Niacinamide / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects; D013917:Thrombin / Q000494:pharmacology
D009243:NAD; D000246:Adenosine Diphosphate Ribose; D009536:Niacinamide; D009244:NAD+ Nucleosidase; D013917:Thrombin; D000241:Adenosine