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Cardiovascular Research 2001 51(3):463-469; doi:10.1016/S0008-6363(01)00340-6
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Regulation of mesangial cell function by vasodilatory signaling molecules

Lutz Buschhausen, Stefan Seibold, Oliver Gross, Tilman Matthaeus, Manfred Weber and Eckhard Schulze-Lohoff*

Department of Medicine and Nephrology, Merheim Medical Center, Medical Faculty of Cologne University, D-51109 Cologne, Germany

* Corresponding author. Tel.: +49-221-8907-3200; fax: +49-221-8907-3335 e.schulze-lohoff{at}uni-koeln.de

Proliferation of mesangial cells and expansion of mesangial matrix is a hallmark of glomerular disease leading to end-stage renal failure and requiring renal replacement therapy. Independently from the type of injury, e.g. in glomerulonephritis or diabetic nephropathy, the response to injury is remarkably uniform. Chronic glomerular disease is frequently associated with increases in systemic blood pressure and altered intraglomerular hemodynamics. Furthermore, reduction of systemic blood pressure and inhibition of the vasoconstrictor peptide angiotensin II have been shown to delay end-stage renal failure in various types of human kidney disease. Since vasoconstrictors of mesangial cells and efferent glomerular arterioli, such as angiotensin II, are thought to be detrimental for the progression of chronic glomerular disease, we propose that vasodilatory factors which antagonize the effects of angiotensin II, might have beneficial effects during the course of progressive kidney disease. To support this concept we will summarize currently available data on the role of vasodilatory signaling molecules such as natriuretic peptides (ANP, BNP and CNP), nitric oxide (NO), the prostaglandines PGE2 and prostacycline, and the purine mediator adenosine in the regulation of mesangial function.

KEYWORDS Natriuretic peptide; Nitric oxide; Prostaglandine; Adenosine


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