Effect of Cyclosporin A on prostacyclin synthesis by vascular tissue

G. H. Neild, G. Rocchi, L. Imberti, F. Fumagalli, Z. Brown, G. Remuzzi, D. G. Williams

Research output: Contribution to journalArticlepeer-review


NZW rabbits with acute serum sickness given Cyclosporin A (CyA) 25 mg/kg/day develop glomerular capillary thrombosis similar to that seen in the haemolytic uraemic syndrome (HUS). Bone marrow recipients treated with CyA may also develop a similar renal lesion associated with a haemolytic uraemic-like syndrome. In the HUS, impaired production of prostacyclin by vascular tissue may be found and has been associated with a lack of a plasma factor which stimulates prostacyclin synthesis. We therefore examined, in six normal rabbits, treated with CyA 25 mg/kg for five days, the ability of plasma from treated and untreated rabbits to stimulate prostacyclin synthesis from normal rabbit aortic rings. Plasma from untreated rabbits produced 21.5 ± 6.9ng 6-keto PGFlα/ml/mg wet weight aorta (mean ± SEM). However, the ability of plasma from CyA-treated rabbits to stimulate prostacyclin production was profoundly reduced. This was apparent within 24 hours of starting and persisted for seven days after therapy was stopped: mean of values from all rabbits bled from start of therapy until seven days after therapy stopped was 3.7 ± 0.5ng/ml/mg. We suggest that the renal complications of CyA therapy are related to a failure of normal vascular prostacyclin synthesis due to lack of a prostacyclin-stimulating plasma factor.

Original languageEnglish
Pages (from-to)373-379
Number of pages7
JournalThrombosis Research
Issue number4
Publication statusPublished - Nov 15 1983


  • Cyclosporin A
  • Prostacyclin
  • Vascular endothelium

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Hematology


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