Cyclosporine induced alterations in vasopressin signalling in the glomerular mesangial cell

S. Kremer, B. Margolis, P. Harper, K. Skorecki

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Nephrotoxicity is the major limiting factor in the clinical use of cyclosporine A (CyA), which in its acute form results in a decrease in renal blood flow and glomerular filtration rate. Contractile mesangial cells regulate glomerular capillary patency in response to vasoactive stimuli including vasopressin. Hence the effects of CyA on the cellular signalling mechanism of vasopressin in cultured glomerular mesangial cells were investigated. Vasopressin induced a transient rise in intracellular calcium which was enhanced in the presence of CyA. In addition, CyA decreased both basal and vasopressin stimulated PGE2 production. This inhibition was mediated at least in part at the level of arachidonate release and may involve inhibition of phospholipase A2. We conclude that the increased renal and systemic vasoconstriction that occurs with CyA treatment may be the result of an exaggerated rise in intracellular calcium obtained with diminished production of vasorelaxant prostaglandins in response to vasoconstrictor hormones.

Original languageEnglish
Pages (from-to)201-206
Number of pages6
JournalClinical and Investigative Medicine
Issue number3
StatePublished - 1989
Externally publishedYes


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