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Basic Research |
1 Department of Nephrology, Medizinische Poliklinik - Innenstadt; 2 Department of Surgery - Innenstadt, Klinikum der Universität München, München, Germany
Correspondence to: M. Sauter, Medizinische Poliklinik-Innenstadt, Klinikum der
Universitaet Muenchen, Petten-koferstr. 8a, 80336 München,
Germany.
Matthias.Sauter{at}med.uni-muenchen.de
Objective: Human mesothelial cells (HMC) are a major
source of intraperitoneal vascular endothelial growth factor (VEGF) and by
that are presumably involved in complications of long-term peritoneal dialysis
(PD), such as ultrafiltration failure. This prompted us to look for agents
that reduce basic mesothelial VEGF production and abrogate VEGF-overproduction
induced by proinflammatory cytokines such as tumor necrosis factor alpha
(TNF-
) and interleukin-1 (IL-1). Angiotensin-converting
enzyme (ACE) inhibition was found to preserve peritoneal function and
ameliorate morphologic changes in a rat PD model. The present in
vitro study was designed to investigate the effect of the ACE inhibitors
captopril and enalapril, and the angiotensin II type 1-receptor (AT1)
antagonist losartan on mesothelial VEGF synthesis. Methods: HMC were isolated from omental tissue and taken
into culture. VEGF antigen concentrations were measured in the cell
supernatant by ELISA. VEGF mRNA levels were determined by real-time polymerase
chain reaction. Results: Incubation of HMC with captopril (100-1000
µmol/L) resulted in a concentration-dependent attenuation of VEGF
synthesis. Incubation with captopril (500-1000 µmol/L), enalapril (100-1000
µmol/L), and losartan (1-100 µmol/L) significantly decreased
inflammatory mediator (TNF-, IL-1)-induced mesothelial VEGF
overproduction. Conclusion: The results indicate that ACE inhibitors and
AT1-receptor blockers are capable of effectively attenuating the
overproduction of VEGF due to proinflammatory cytokine stimuli. These data
suggest that locally produced angiotensin II in the peritoneal cavity may be a
potential therapeutic target in ultrafiltration failure during longterm
PD.
KEY WORDS: KEY WORDS:; Mesothelial cells; vascular endothelial growth factor; ACE inhibitor; AT1-receptor blocker.
Received 20 October 2006; accepted 12 January 2007.
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