Increased glomerular capillary pressure alters glomerular cytokine expression

Abstract

Increased glomerular capillary hydrostatic pressure (PGC) is an important hemodynamic determinant of glomerular injury, but the molecular events responsible for this association are poorly understood. PGC is normal in spontaneously hypertensive rats (SHR), but uninephrectomy leads to an increase in PGC and accelerated glomerulosclerosis. Since recent studies have implicated transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor (PDGF) in the pathogenesis of glomerulosclerosis, we first sought to determine if uninephrectomy increased mRNA levels for TGF-β1 and PDGF in glomeruli of SHR. Since treatment with the angiotensin-converting enzyme (ACE) inhibitor enalapril lowers PGC and prevents glomerulosclerosis in uninephrectomized SHR, we also sought to determine if ACE inhibitor lowered mRNA levels for TGF-β1 and PDGF in the glomeruli of uninephrectomized SHR. PGC increased from 53±1 to 64±1 mm Hg 1 week after uninephrectomy in SHR (P