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Updated: Aug 7, 2026

In vitro Measurements of Tracheal Constriction Using Mice
10:20

In vitro Measurements of Tracheal Constriction Using Mice

Published on: June 25, 2012

Ca2+-activated K+ channel blockers induce PKC modulated oscillatory contractions in guinea pig trachea

Yukihiro Yagi1, Masayoshi Kuwahara, Hirokazu Tsubone

  • 1Department of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan.

Comparative Biochemistry and Physiology. Toxicology & Pharmacology : CBP
|April 27, 2002
PubMed

Insights

Calcium-activated potassium channel (K(Ca)) blockers trigger oscillatory contractions in guinea pig trachea, initiated by calcium influx via L-type channels and modulated by protein kinase C.

Area of Science:

  • Pharmacology
  • Physiology
  • Smooth Muscle Biology

Background:

  • Calcium-activated potassium channels (K(Ca)) play a crucial role in regulating smooth muscle function.
  • Understanding the mechanisms of K(Ca) channel blocker-induced contractions is vital for respiratory research.

Purpose of the Study:

  • To investigate the underlying mechanisms of oscillatory contractions induced by K(Ca) channel blockers in guinea pig tracheal smooth muscle.
  • To elucidate the roles of calcium influx pathways and intracellular calcium release in these contractions.

Main Methods:

  • Utilized charybdotoxin (ChTX) and iberiotoxin (IbTX) to induce oscillatory contractions.
  • Assessed the effects of various calcium channel blockers (nifedipine, SK&F 96365), ryanodine, thapsigargin, and protein kinase C (PKC) modulators.

Main Results:

  • ChTX and IbTX induced dose-dependent oscillatory contractions.
  • Contractions were dependent on extracellular calcium and abolished by L-type calcium channel blockers.
  • Ryanodine affected contraction amplitude and frequency, while thapsigargin induced sustained contractions.
  • PKC inhibition decreased, while activation increased, oscillatory contraction parameters.

Conclusions:

  • K(Ca) inhibitors induce oscillatory contractions primarily through calcium influx via L-type voltage-dependent calcium channels.
  • Ryanodine-sensitive calcium release channels in the sarcoplasmic reticulum are important for maintaining these oscillations.
  • Protein kinase C activity modulates the frequency and amplitude of these contractions.

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