Captopril-induced granulocyte aggregation. A possible complement mediated mechanism of peripheral leukopenia.
Captopril, competitive inhibitor of angiotensin converting enzyme, is clinically employed for its antihypertensive activity and drug-dependent granulocytopenia or agranulocytosis have been seldom observed during treatment. In previous unpublished studies an activating effect of the drug on the complement alternate pathway has been demonstrated. In this paper we demonstrate that captopril-treated serum is able to "in vitro" induce granulocyte activation and aggregation. Granulocyte aggregation was shown by the turbidimetric method and cellular activation was confirmed by the release of the granule associated enzyme lysozyme and beta-glucuronidase. On this basis complement-mediated leukoaggregation and leukosequestration in vivo could be proposed as the effector mechanism of peripheral leukopenia.
D002216:Captopril / Q000494:pharmacology*; D002449:Cell Aggregation / Q000187:drug effects; D002469:Cell Separation; D003167:Complement Activation; D003571:Cytochalasin B / Q000494:pharmacology; D005966:Glucuronidase / Q000378:metabolism; D006098:Granulocytes / Q000276:immunology*; D006801:Humans; D007444:Inulin / Q000494:pharmacology; D007970:Leukopenia / Q000139:chemically induced / Q000276:immunology*; D009113:Muramidase / Q000378:metabolism; D011392:Proline / Q000031:analogs & derivatives*
D003571:Cytochalasin B; D007444:Inulin; D011392:Proline; D002216:Captopril; D009113:Muramidase; D005966:Glucuronidase