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pmid19384836      J+Nephrol 2009 ; 22 (2): 196-202
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  • Disturbances of glomerular hemodynamics: a risk factor determing progression of glomerular diseases? #MMPMID19384836
  • Oite T; Yao J
  • J Nephrol 2009[Mar]; 22 (2): 196-202 PMID19384836show ga
  • In this review, we introduce first our experimental rat model in which disturbances of vascular regeneration and glomerular hemodynamics lead to irreversible glomerulosclerosis. Secondly, we demonstrate a pivotal role for gap-junctional intercellular communication and adenosine triphosphate-dependent intercellular communication, via Ca++ signaling, in coordinating behavior of mesangial and juxtaglomerular cells. This has deepened our understanding of regulatory glomerular hemodynamics at the cellular and molecular levels. Thirdly, we show that local delivery of renoprotective agents such as angiotensin II receptor blockers, in combination with a diagnostic imaging system of the renal microvasculature, allowed us to evaluate the therapeutic effects of local blockade of renin-angiotensin system activity on the progression of glomerulosclerosis, finally leading to renal death.
  • |Animals[MESH]
  • |Disease Progression[MESH]
  • |Glomerulosclerosis, Focal Segmental/metabolism/*physiopathology[MESH]
  • |Humans[MESH]
  • |Kidney Glomerulus/*blood supply/ultrastructure[MESH]
  • |Microscopy, Electron, Scanning[MESH]
  • |Prognosis[MESH]
  • |Renal Circulation/*physiology[MESH]


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