Regulation of mesangial cell function by vasodilatory signaling molecules

Proliferation of mesangial cells and expansion of mesangial matrix is a hal lmark of glomerular disease leading to end-stage renal failure and requirin g renal replacement therapy. Independently from the type of injury, e.g. in glomerulonephritis or diabetic nephropathy, the response to injury is rema rkably uniform. Chronic glomerular disease is frequently associated with in creases in systemic blood pressure and altered intraglomerular hemodynamics . Furthermore, reduction of systemic blood pressure and inhibition of the v asoconstrictor peptide angiotensin II have been shown to delay end-stage re nal failure in various types of human kidney disease. Since vasoconstrictor s of mesangial cells and efferent glomerular arterioli, such as angiotensin II, are thought to be detrimental for the progression of chronic glomerula r disease, we propose that vasodilatory factors which antagonize the effect s of angiotensin II, might have beneficial effects during the course of pro gressive kidney disease. To support this concept we will summarize currentl y available data on the role of vasodilatory signaling molecules such as na triuretic peptides (ANP, BNP and CNP), nitric oxide (NO), the prostagglandi nes PGE2 and prostacycline, and the purine mediator adenosine in the regula tion of mesangial function. (C) 2001 Elsevier Science BY. All rights reserv ed.