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MAPK and PKC activity are not required for H(2)O(2)-induced arterial muscle contraction

N J Pelaez1, S L Osterhaus, A S Mak

  • 1Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis, Indiana 46202-5120, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|September 20, 2000
PubMed

Insights

Hydrogen peroxide (H2O2) causes pulmonary arterial smooth muscle (PASM) contractions independently of calcium. Mitogen-activated protein kinase (MAPK) activation is not required for these H2O2-induced PASM contractions.

Area of Science:

  • Physiology
  • Biochemistry
  • Pharmacology

Background:

  • Pulmonary arterial smooth muscle (PASM) contractions are crucial for regulating vascular tone.
  • Hydrogen peroxide (H2O2)-induced PASM contractions are known to be independent of intracellular calcium (Ca2+) and myosin light chain phosphorylation.
  • The precise signaling pathways mediating H2O2-induced PASM contractions remain incompletely understood.

Purpose of the Study:

  • To investigate the potential involvement of mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) in H2O2-induced PASM contractions.
  • To determine if MAPK or PKC activation is a prerequisite for the development of force in PASM stimulated by H2O2.

Main Methods:

  • Porcine PASM strips were utilized for mechanical tension measurements.
  • Stimulation was performed using H2O2, high potassium (KCl), or phorbol myristic acetate (PMA).
  • MAPK phosphorylation and PKC activity were assessed at various time points during contraction using biochemical assays and Western blotting.

Main Results:

  • MAPK tyrosine phosphorylation levels increased in parallel with tension development.
  • Inhibition of MAPK activation with PD-98059 did not alter the magnitude of H2O2-induced isometric tension.
  • PKC activity did not correlate with the time course of force generation in response to H2O2.

Conclusions:

  • MAPK activation is not essential for H2O2-induced PASM contractions.
  • MAPK activation may be a downstream event or a consequence of contraction induced by various agonists, rather than a primary driver for H2O2-induced contractions.
  • These findings suggest alternative signaling mechanisms are responsible for H2O2-mediated PASM contraction.

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