By Kihito Takahashi, Tetsuo Katoh, Kamal F. Badr (auth.), Vittorio E. Andreucci, Leon G. Fine (eds.)
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Extra info for International Yearbook of Nephrology 1991
Klahr S, Schreiner G, Ichikawa I: The progression ofrenal disease. New Engl J Med, 318: 16571666, 1988. Grond J, Koudstaal J, Elema JD: Mesangial function and glomerular sclerosis in rats with aminonucleoside nephrosis. Kidney lnt, 27 :405-410, 1985. KIahr S, Heifets M, Purkerson ML: The influence of anticoagulation on the progression of experimental renal disease. In: "The progressive nature of renal disease" ( Ed WE Mitch, BM Brenner, JH Stein), Churchill Livingstone, New York, 1986, pp 45-64.
In addition to anticoagulant effects, these agents may regulate the proliferation of glomerular cells. In this regard, since platelet aggregation is followed by release of its products, it can be envisioned that inhibition of platelet aggregation will abolish this growth-promoting effect by preventing release of pDGF and other active substances. Heparin, which is released locally within the glomerulus, is of particular interest, since administration of heparin in subtotally nephrectomized animals markedly attenuated the progression of glomerular sclerosis (61).
Brenner BM, Troy JL, Ballermann BJ: Endothelium-dependent vascular responses. J Clin lnvest, 84: 1373-1378, 1989. Shultz PJ, Sehorer AE, Raij L: Effeets of endothelium-derived relaxing factor and nitrie oxide on rat mesangial eells. Am J Physiol, 258: FI62-FI67, 1990. Marsden PA, Brock TA, Ballermann BJ: Glomerular endothelial cells respond to calcium mobilizing agonists with release of endothelium derived relaxing factor. Clin Res, 37: 496A, 1989. Marsden PA, Ballermann BJ: Tumor necrosis factor activates soluble guanylate cyclase in bovine glomerular mesangial cells via an L-arginine-dependent mechanism.