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Updated: Sep 30, 2026

In vitro Measurements of Tracheal Constriction Using Mice
Published on: June 25, 2012
The influence of different InsP(3) receptor isoforms on Ca(2+) signaling in tracheal smooth muscle cells
Thomas Haberichter1, Etienne Roux, Marko Marhl
1Theoretical Biophysics, Institute of Biology, Humboldt University Berlin, Invalidenstr. 43, 10115 Berlin, Germany. thomas@gnsbiotech.com
Abstract:
In airway myocytes, like in many cells, Ca(2+) signaling is controlled by inositol 1,4,5-trisphosphate (InsP(3)) via InsP(3) receptors (InsP(3)R) located in the sarco-endoplasmic reticulum. Three types of InsP(3)R exist, labeled Types 1, 2, and 3, which differ in their gating kinetics. We analyze a possible impact of the different gating kinetics of Type 1 and Type 3 InsP(3)R on the time course of cytosolic Ca(2+) concentration in tracheal smooth muscle cells upon agonist stimulation. Previous experimental data in rat tracheal myocytes showed that upon gradually increased stimulation with acetylcholine (ACh), a contractile agonist that acts via InsP(3) production, signal spikes, several spikes with declining maxima, and sustained oscillations appear. Our model reproduces the time courses of cytosolic Ca(2+) measured in tracheal myocytes. Moreover, by postulating slight variations in the model parameters which determine the total number of receptors expressed and the ratio between Type 1 and Type 3 InsP(3)R, it offers an explanation to the experimental observation of qualitatively different responses of cells within a presumably homogeneous tissue.
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