Beneficial effects of a combination of Rho-kinase inhibitor and ACE inhibitor on tubulointerstitial fibrosis induced by unilateral ureteral obstruction

Hypertens Res. 2010 Sep;33(9):965-73. doi: 10.1038/hr.2010.112. Epub 2010 Jul 22.

Abstract

We and others recently reported that long-term Rho-kinase inhibition has renoprotective effects. This study was designed to compare the effects of an angiotensin-converting enzyme (ACE) inhibitor (imidapril), a Rho-kinase inhibitor (fasudil) and a combination of them both on renal interstitial fibrosis induced by unilateral ureteral obstruction (UUO). We also attempted to elucidate the mechanism involved. Imidapril (50 mg l(-1)), fasudil (1 g l(-1)) or a combination of them both was given in drinking water to mice, and their effects were compared on renal interstitial fibrosis induced by UUO. We assessed histological findings, monocyte/macrophage infiltration, myofibroblast differentiation, oxidative stress and the expression of various mRNA in the kidney by UUO. Eleven days after UUO, wild-type kidney was characterized by increased fibrotic area, dihydroethidium (DHE)-positive area, alpha-smooth muscle actin (SMA)-positive area, F4/80-positive area and the increased expression of various mRNA. Fasudil and imidapril similarly improved fibrotic area (-23%, -15%), DHE-positive area (-13%, -11%), alpha-SMA-positive area (-22%, -15%), F4/80-positive area (-42%, -34%) and the expression of various mRNA, most of which were significant (P<0.05). The combination of imidapril and fasudil further improved fibrotic area (-52%), DHE-positive area (-26%), alpha-SMA-positive area (-33%), F4/80-positive area (-62%) and the expression of various mRNA (all P<0.05 vs. monotherapy). Compared with either agent alone, the combination of an ACE inhibitor and a Rho-kinase inhibitor was more effective for the prevention of renal interstitial fibrosis because of the inhibition of transforming growth factor-beta/collagen, monocyte/macrophage infiltration, myofibroblast differentiation, inflammation and the oxidative stress pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / analogs & derivatives*
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / therapeutic use
  • Actins / analysis
  • Angiotensin-Converting Enzyme Inhibitors / pharmacology
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
  • Animals
  • Antigens, Differentiation / analysis
  • Cell Differentiation / drug effects
  • Drug Therapy, Combination
  • Ethidium / analogs & derivatives
  • Ethidium / analysis
  • Imidazolidines / pharmacology
  • Imidazolidines / therapeutic use*
  • Macrophages / drug effects
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Myofibroblasts / drug effects
  • Nephritis, Interstitial / drug therapy*
  • Nephritis, Interstitial / etiology
  • Nephritis, Interstitial / metabolism
  • Nephritis, Interstitial / pathology
  • Oxidative Stress / drug effects
  • Ureteral Obstruction / complications
  • rho-Associated Kinases / antagonists & inhibitors*

Substances

  • Actins
  • Angiotensin-Converting Enzyme Inhibitors
  • Antigens, Differentiation
  • Imidazolidines
  • alpha-smooth muscle actin, mouse
  • monocyte-macrophage differentiation antigen
  • dihydroethidium
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • imidapril
  • rho-Associated Kinases
  • Ethidium
  • fasudil