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The effect of chronic nitric oxide synthases inhibition on regulatory proteins in rat hearts

Anna Spániková1, Petra Simoncíková, Tána Ravingerová

  • 1Institute for Heart Research, Centre of Excellence for Cardiovascular Research, Slovak Academy of Sciences, Dúbravská cesta 9, P.O. Box 104, 840 05 Bratislava, Slovak Republic.

Molecular and Cellular Biochemistry
|March 11, 2008
PubMed

Insights

Chronic nitric oxide deficiency in rats reduced key signaling proteins in heart muscle, impacting pathways like ERK and Akt kinase. These findings suggest a link between nitric oxide, these pathways, and heart responses.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) plays a crucial role in cardiovascular regulation.
  • Dysregulation of NO signaling is implicated in various heart conditions.
  • Intracellular signaling pathways and matrix metalloproteinases are vital in myocardial function.

Purpose of the Study:

  • To investigate the impact of chronic nitric oxide synthase (NOS) inhibition on myocardial regulatory proteins.
  • To analyze alterations in mitogen-activated protein kinase (MAPK) and Akt kinase signaling cascades.
  • To assess changes in matrix metalloproteinase (MMP) activities in response to nitric oxide deficiency.

Main Methods:

  • Induction of chronic NO deficiency (NOD) using NG-nitro-L-arginine methyl ester (L-NAME) in rats for 4 weeks.
  • Quantification of protein levels and kinase activation via Western blot and specific antibodies.
  • Analysis of MMP activities using zymography with gelatin-containing gels.

Main Results:

  • NOD was associated with reduced endothelial NOS (eNOS) activation and inducible NOS (iNOS) protein levels.
  • L-NAME treatment decreased the activation of extracellular signal-regulated kinases (ERK) and Akt kinase.
  • Activities of tissue MMP-2 were found to be decreased in L-NAME-treated rat hearts.

Conclusions:

  • Chronic NO deficiency leads to the inhibition of ERK and Akt kinase pathways in the myocardium.
  • These signaling pathway alterations suggest their involvement in the heart's response to NOD.
  • A potential relationship exists between ERK, Akt kinase pathways, eNOS activation, and MMP-2 activity.

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