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Role of ERK1/2 signaling pathways in 4-aminopyridine-induced rat pulmonary vasoconstriction

Weina Han1, Xiaobo Tang, Hong Wu

  • 1College of Pharmacy, Harbin Medical University, 157 Baojian Road, Nangang District, Harbin, Heilongjiang 150081, P.R. of China.

European Journal of Pharmacology
|June 1, 2007
PubMed

Insights

Extracellular signal regulated kinase-1/2 (ERK1/2) signaling contributes to pulmonary artery contraction caused by 4-aminopyridione (4-AP). Inhibiting ERK1/2 reduces 4-AP-induced vasoconstriction and phosphorylation of ERK1/2 in pulmonary artery smooth muscle cells.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Pharmacology

Background:

  • Pulmonary vascular tone is regulated by voltage-gated K(+) channels.
  • 4-aminopyridione (4-AP) inhibits these channels, affecting pulmonary artery contraction.
  • The role of extracellular signal regulated kinase-1/2 (ERK1/2) in this process requires elucidation.

Purpose of the Study:

  • To investigate the contribution of the ERK1/2 signaling pathway to pulmonary artery contraction induced by 4-AP.
  • To examine the effect of 4-AP on the expression of phosphorylated ERK1/2 (p-ERK1/2) in pulmonary arterial smooth muscle cells (PASMCs) and tissues.

Main Methods:

  • Isolated rat pulmonary artery rings were used to measure tension changes.
  • ERK1/2 inhibitors (PD98059, U0126) were employed to block ERK1/2 activation.
  • Western blotting was used to assess p-ERK1/2 expression in PASMCs and whole tissues.

Main Results:

  • 4-AP caused a concentration-dependent increase in pulmonary artery ring tension.
  • Pretreatment with ERK1/2 inhibitors PD98059 and U0126 significantly reduced 4-AP-induced vasoconstriction.
  • 4-AP increased p-ERK1/2 expression in PASMCs and tissues, an effect blocked by U0126.

Conclusions:

  • The ERK1/2 signaling pathway plays a significant role in mediating pulmonary vasoconstriction induced by 4-AP.
  • These findings highlight ERK1/2 as a potential target for modulating pulmonary vascular tone.

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