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Mitogen-activated protein kinase plays an important role in hemolysate-induced contraction in rabbit basilar artery

A Y Zubkov1, K Ogihara, A Patllola

  • 1Department of Neurosurgery, University of Mississippi Medical Center, Jackson, Mississippi, USA.

Acta Neurochirurgica. Supplement
|July 14, 2001
PubMed
Abstract

Insights

Mitogen-activated protein kinase (MAPK) activation by hemolysate causes rabbit basilar artery contraction. Inhibiting MAPK may treat cerebral vasospasm after subarachnoid hemorrhage.

Area of Science:

  • Vascular biology
  • Neuroscience
  • Pharmacology

Background:

  • Cerebral vasospasm, characterized by vascular proliferation and contraction, is a critical complication of subarachnoid hemorrhage.
  • Mitogen-activated protein kinase (MAPK) signaling is implicated in vascular dynamics relevant to vasospasm.

Purpose of the Study:

  • To investigate the role of MAPK in hemolysate-induced signal transduction and contraction in rabbit basilar arteries.
  • To determine if MAPK activation mediates the contractile response to hemolysate.

Main Methods:

  • Isometric tension recordings were used to measure rabbit basilar artery contractile responses to hemolysate.
  • Western blotting was employed to assess MAPK activation following hemolysate exposure.
  • The effects of the MAPK kinase inhibitor PD-98059 on hemolysate-induced contraction and MAPK activation were evaluated.

Main Results:

  • Hemolysate induced a concentration-dependent contraction of rabbit basilar arteries.
  • Pre-incubation with PD-98059 significantly attenuated hemolysate-induced contraction and relaxed sustained contractions.
  • Hemolysate exposure led to a time-dependent increase in MAPK immunoreactivity, peaking at 5 minutes and remaining elevated for at least two hours.
  • PD-98059 pre-incubation blocked the hemolysate-induced elevation of MAPK.

Conclusions:

  • Hemolysate triggers contraction in rabbit basilar arteries, likely through MAPK activation.
  • MAPK pathway inhibition presents a potential therapeutic strategy for managing cerebral vasospasm.

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