ROLES OF NITRIC-OXIDE AND OF NO-ANTAGONIS TS IN EXPERIMENTAL GLOMERULONEPHRITIS

Endogenous nitric oxide is known to cause vasodilatation, inhibition o f platelet aggregation, and cytotoxicity to cells and microorganisms i n specific circumstances. These different properties are the results o f activation of several different NO-synthases. Presently available NO -antagonists - including aminoguanidine - inhibit these NO-synthases i n a non-specific manner. Therefore the use of NO-antagonists will be a ssociated with side - effects such as arterial hypertension, platelet aggregation and possibly bacterial overgrowth. Several models of nephr otoxic-serum induced glomerulonephritis have been used in studies of t he potential role (s) of NO in nephritis. It has been found that NO is highly significantly stimulated during the phase of macrophage depend ent induction of nephritis. However inhibition of this NO worsened the nephritis in 3 out of 4 reported studies. It was suggested that NO ac ted in a protective fashion in those studies. Recently a study of huma n renal biopsy material has indicated that NO-synthase is induced in I gA-nephropathy.