NITRIC OXIDE AVAILABILITY AS KEY REGULATOR IN THE DEVELOPING KIDNEY

WALTER MANUCHA

Tafí del Valle, Tucumán

Congreso; XXVIII Jornadas Científicas de la Asociación de Biología de Tucumán; 2011

Asociación de Biología de Tucumán

Congenital obstructive nephropathy is the primary cause of end-stage renal disease in children. Rapid diagnosis and initiation of the treatment are vital to preserve function and/or to slow down renal injury. Obstructive uropathy effects -decline in the plasmatic renal flow and glomerular filtration rate, interstitial infiltrate of leukocytes, significant decrease in urine concentration, loss of the capacity to concentrate urine as well as fibrosis and apoptosis- are a consequence of a variety of factors that work in complex ways and are still not fully understood. Experimental neonatal obstruction in rodents can be used as a paradigm for in utero obstruction in humans and the potential of novel therapies for congenital obstructive nephropathy can be explored therein. Mediators such as angiotensin II, transforming growth factor beta, heat shock response and nitric oxide (NO) have been implicated in congenital obstructive nephropathy. NO has emerged as an important endogenous inhibitor of apoptosis. The functional integrity of the kidney depends on normal development as well as on physiological cell turnover. Apoptosis induction is essential for these mechanisms. Multiple mechanisms are unleashed during obstructive nephropathy, one of the most complex being programmed cell death that leads to renal tubular atrophy and tubular loss. This presentation will focus on the interaction between nitric oxide and Hsp70 and on the regulation of renal antiapoptotic/antifibrotic and protective oxidative stress responses. in utero obstruction in humans and the potential of novel therapies for congenital obstructive nephropathy can be explored therein. Mediators such as angiotensin II, transforming growth factor beta, heat shock response and nitric oxide (NO) have been implicated in congenital obstructive nephropathy. NO has emerged as an important endogenous inhibitor of apoptosis. The functional integrity of the kidney depends on normal development as well as on physiological cell turnover. Apoptosis induction is essential for these mechanisms. Multiple mechanisms are unleashed during obstructive nephropathy, one of the most complex being programmed cell death that leads to renal tubular atrophy and tubular loss. This presentation will focus on the interaction between nitric oxide and Hsp70 and on the regulation of renal antiapoptotic/antifibrotic and protective oxidative stress responses.