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Nephrotoxicity of cyclosporine: The role of platelet‐activating factor and thromboxane
Author(s) -
Pavão dos Santos Oscar F.,
Boim Mirian A.,
Barros Elvino J. G.,
Pirotzky Eduardo,
Braquet Pierre,
Schor Nestor
Publication year - 1991
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02536557
Subject(s) - nephrotoxicity , thromboxane , pharmacology , renal function , platelet activating factor , chemistry , medicine , endocrinology , kidney , platelet
Cyclosporine (CsA), an immunosuppressive agent, is potentially nephrotoxic. We had previously observed that acute administration of CsA to Munich‐Wistar rats induced a decrease in single nephron glomerular filtration rate, due to a decline in glomerular plasma flow, and in the glomerular ultrafiltration coefficient. Moreover, these alterations were prevented when an antagonist of platelet‐activating factor (PAF) was administered. In the present study we examined whether the protective effect of the PAF blocker in CsA nephrotoxicity could have been mediated by thromboxane (TxA 2 ). Our data show that the PAF effects were not mediated by TxA 2 , since administration of dazmegrel, a thromboxane synthetase inhibitor, did not ameliorate the acute renal failure caused by CsA. Thus, PAF appears to be a direct mediator of acute CsA nephrotoxicity, while TxA 2 is not significantly involved in this process.