Effects of a Novel Histone Deacetylase Inhibitor, N-(2-Aminophenyl) Benzamide, on a Reversible Hypertrophy Induced by Isoproterenol in In Situ Rat Hearts

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Author(s)

Abstract

The aim of the present study was performed to determine whether a novel histone deacetylase (HDAC) inhibitor, <i>N</i>-(2-aminophenyl)-4-{[benzyl(2-hydroxyethyl)amino]methyl} benzamide (K-183), prevents a reversible cardiac hypertrophy induced by isoproterenol and improves left ventricular (LV) dysfunction in rats. Either isoproterenol or vehicle was infused for 3 days by osmotic minipump. One hour prior to the implantation of isoproterenol, K-183 or trichostatin A (TSA) was injected twice a day for 3 days. We recorded continuous LV pressure-volume (P-V) loops of in situ hearts one hour after removal of the osmotic minipump. LV work capability (systolic P-V area at midrange LV volume: PVA<sub>mLVV</sub>) and hemodynamics were evaluated. K-183 per se induced neither cardiac hypertrophy nor collagen production. Although K-183 did not prevent the hypertrophy, where PVA<sub>mLVV</sub> remained decreased, K-183, differently from TSA, significantly attenuated the decrease of cardiac output and the increase of effective arterial elastance in the hypertrophied heart. These results indicate that the novel HDAC inhibitor K-183 has some beneficial effects on hemodynamics, although K-183 has no effects of anti-hypertrophic modalities.<br>

Journal

  • Journal of Pharmacological Sciences

    Journal of Pharmacological Sciences 104(2), 167-175, 2007-06-20

    The Japanese Pharmacological Society

References:  36

Cited by:  2

Codes

  • NII Article ID (NAID)
    10024314451
  • NII NACSIS-CAT ID (NCID)
    AA11806667
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    13478613
  • NDL Article ID
    8781911
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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