@entity842 (NO), an @entity534 derivative, is implicated in neuronal transmission, immune response and vasodilation, besides acting as a platelet function modulator. A number of recent studies in the experimental model of renal mass reduction (RMR) in @entity35 have proposed the hypothesis that abnormalities of the NO synthetic pathway could have a key role in mediating the complex hemodynamic and @entity4461 associated with the progression of @entity8 . Thus, renal NO generation is lower than normal in @entity35 with RMR seven days after surgery, and progressively worsens with time in close correlation with signs of @entity8 . This abnormality is due to a strong defect of @entity1506 ( @entity1506 ) content in the kidney. In the same model, administration of either the NO precursor, @entity534 , or a NO-releasing compound reduces @entity644 , slows @entity8 progression and prolongs survival. On the other hand RMR is associated with a progressive increase of renal synthesis of the potent vasoconstrictor peptide, @entity1827 ( @entity1827 ), whose mRNA is expressed in excessive amounts in cortical tubules early after surgical ablation. In this setting, a marked reduction of NO, in the face of continuous local generation of @entity1827 , may well contribute to intraglomerular capillary @entity101 and cell proliferation. Actually, administration of a selective ETA receptor antagonist to RMR @entity35 reduced abnormal permeability to proteins and @entity177 . In the same model the ETA receptor antagonist also corrected the impaired renal NO synthesis, suggesting that excessive @entity1827 bioactivity might also be responsible for the progressive reduction of renal NO. In keeping with this possibility are recent in vitro data that @entity1827 inhibits @entity1506 transcription, a process mediated by interaction of the peptide with subtype A receptors. @entity842 and @entity1827 have profound and opposite effects on glomerular and tubular function. Thus, abnormalities of renal NO and @entity1827 synthetic pathways, as documented in the RMR model, likely have major and complementary roles in promoting alteration in renal hemodynamics and functions in progressive @entity8 .

XXXX /endothelin balance after nephron reduction.

@entity644 :: ('MESH:D011507', 'Disease') :: ['proteinuria'] @entity8 :: ('MESH:D007674', 'Disease') :: ['nephropathies', 'renal disease', 'renal injury'] @entity101 :: ('MESH:D006973', 'Disease') :: ['hypertension'] @entity1506 :: ('24599(Tax:10116)', 'Gene') :: ['inducible NO synthase', 'iNOS'] @entity534 :: ('CHEBI:16467', 'Chemical') :: ['L-arginine'] @entity177 :: ('MESH:D051437', 'Disease') :: ['prevented renal function deterioration'] @entity842 :: ('MESH:D009569', 'Chemical') :: ['Nitric oxide'] @entity4461 :: ('MESH:D020141', 'Disease') :: ['hemostatic disorders'] @entity1827 :: ('24323(Tax:10116)', 'Gene') :: ['ET-1', 'endothelin-1'] @entity35 :: ('10116', 'Species') :: ['rats']
@entity842 :: (MESH:D009569,Chemical) :: ['Nitric oxide']
