Impairment of Ca2+ mobilization in circular muscle cells of the inflamed colon

Xuan-Zheng Shi, Sushil K. Sarna

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

This study investigated whether inflammation modulates the mobilization of Ca2+ in canine colonic circular muscle cells. The contractile response of single cells from the inflamed colon was significantly suppressed in response to ACh, KCl, and BAY K8644. Methoxyverapamil and reduction in extracellular Ca2+ concentration dose-dependently blocked the response in both normal and inflamed cells. The increase in intracellular Ca2+ concentration in response to ACh and KCl was significantly reduced in the inflamed cells. However, Ca2+ efflux from the ryanodine- and inositol 1,4,5-trisphosphate (IP3)-sensitive stores, as well as the decrease of cell length in response to ryanodine and IP3, were not affected. Heparin significantly blocked Ca2+ efflux and contraction in response to ACh in both conditions. ACh-stimulated accumulation of IP3 and the binding of [3H]ryanodine to its receptors were not altered by inflammation. Ruthenium red partially inhibited the response to ACh in normal and inflamed states. We conclude that the canine colonic circular muscle cells utilize Ca2+ influx through L-type channels as well as Ca2+ release from the ryanodine- and IP3-sensitive stores to contract. Inflammation impairs Ca2+ influx through L-type channels, but it may not affect intracellular Ca2+ release. The impairment of Ca2+ influx may contribute to the suppression of circular muscle contractility in the inflamed state.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume278
Issue number2 41-2
StatePublished - Feb 2000
Externally publishedYes

Fingerprint

Ryanodine
Muscle Cells
Colon
Inflammation
Canidae
Gallopamil
Ruthenium Red
Inositol 1,4,5-Trisphosphate
Heparin
Muscles

Keywords

  • Acetylcholine
  • Calcium
  • Calcium influx
  • Inflammatory bowel disease
  • Inositol 1,4,5-trisphosphate
  • Intracellular calcium stores
  • Motility
  • Ryanodine
  • Signal transduction
  • Smooth muscle

ASJC Scopus subject areas

  • Gastroenterology
  • Physiology
  • Physiology (medical)

Cite this

Impairment of Ca2+ mobilization in circular muscle cells of the inflamed colon. / Shi, Xuan-Zheng; Sarna, Sushil K.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 278, No. 2 41-2, 02.2000.

Research output: Contribution to journalArticle

@article{89cc70e7c78f4990ad6e4354b19357e9,
title = "Impairment of Ca2+ mobilization in circular muscle cells of the inflamed colon",
abstract = "This study investigated whether inflammation modulates the mobilization of Ca2+ in canine colonic circular muscle cells. The contractile response of single cells from the inflamed colon was significantly suppressed in response to ACh, KCl, and BAY K8644. Methoxyverapamil and reduction in extracellular Ca2+ concentration dose-dependently blocked the response in both normal and inflamed cells. The increase in intracellular Ca2+ concentration in response to ACh and KCl was significantly reduced in the inflamed cells. However, Ca2+ efflux from the ryanodine- and inositol 1,4,5-trisphosphate (IP3)-sensitive stores, as well as the decrease of cell length in response to ryanodine and IP3, were not affected. Heparin significantly blocked Ca2+ efflux and contraction in response to ACh in both conditions. ACh-stimulated accumulation of IP3 and the binding of [3H]ryanodine to its receptors were not altered by inflammation. Ruthenium red partially inhibited the response to ACh in normal and inflamed states. We conclude that the canine colonic circular muscle cells utilize Ca2+ influx through L-type channels as well as Ca2+ release from the ryanodine- and IP3-sensitive stores to contract. Inflammation impairs Ca2+ influx through L-type channels, but it may not affect intracellular Ca2+ release. The impairment of Ca2+ influx may contribute to the suppression of circular muscle contractility in the inflamed state.",
keywords = "Acetylcholine, Calcium, Calcium influx, Inflammatory bowel disease, Inositol 1,4,5-trisphosphate, Intracellular calcium stores, Motility, Ryanodine, Signal transduction, Smooth muscle",
author = "Xuan-Zheng Shi and Sarna, {Sushil K.}",
year = "2000",
month = "2",
language = "English (US)",
volume = "278",
journal = "American Journal of Physiology - Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "2 41-2",

}

TY - JOUR

T1 - Impairment of Ca2+ mobilization in circular muscle cells of the inflamed colon

AU - Shi, Xuan-Zheng

AU - Sarna, Sushil K.

PY - 2000/2

Y1 - 2000/2

N2 - This study investigated whether inflammation modulates the mobilization of Ca2+ in canine colonic circular muscle cells. The contractile response of single cells from the inflamed colon was significantly suppressed in response to ACh, KCl, and BAY K8644. Methoxyverapamil and reduction in extracellular Ca2+ concentration dose-dependently blocked the response in both normal and inflamed cells. The increase in intracellular Ca2+ concentration in response to ACh and KCl was significantly reduced in the inflamed cells. However, Ca2+ efflux from the ryanodine- and inositol 1,4,5-trisphosphate (IP3)-sensitive stores, as well as the decrease of cell length in response to ryanodine and IP3, were not affected. Heparin significantly blocked Ca2+ efflux and contraction in response to ACh in both conditions. ACh-stimulated accumulation of IP3 and the binding of [3H]ryanodine to its receptors were not altered by inflammation. Ruthenium red partially inhibited the response to ACh in normal and inflamed states. We conclude that the canine colonic circular muscle cells utilize Ca2+ influx through L-type channels as well as Ca2+ release from the ryanodine- and IP3-sensitive stores to contract. Inflammation impairs Ca2+ influx through L-type channels, but it may not affect intracellular Ca2+ release. The impairment of Ca2+ influx may contribute to the suppression of circular muscle contractility in the inflamed state.

AB - This study investigated whether inflammation modulates the mobilization of Ca2+ in canine colonic circular muscle cells. The contractile response of single cells from the inflamed colon was significantly suppressed in response to ACh, KCl, and BAY K8644. Methoxyverapamil and reduction in extracellular Ca2+ concentration dose-dependently blocked the response in both normal and inflamed cells. The increase in intracellular Ca2+ concentration in response to ACh and KCl was significantly reduced in the inflamed cells. However, Ca2+ efflux from the ryanodine- and inositol 1,4,5-trisphosphate (IP3)-sensitive stores, as well as the decrease of cell length in response to ryanodine and IP3, were not affected. Heparin significantly blocked Ca2+ efflux and contraction in response to ACh in both conditions. ACh-stimulated accumulation of IP3 and the binding of [3H]ryanodine to its receptors were not altered by inflammation. Ruthenium red partially inhibited the response to ACh in normal and inflamed states. We conclude that the canine colonic circular muscle cells utilize Ca2+ influx through L-type channels as well as Ca2+ release from the ryanodine- and IP3-sensitive stores to contract. Inflammation impairs Ca2+ influx through L-type channels, but it may not affect intracellular Ca2+ release. The impairment of Ca2+ influx may contribute to the suppression of circular muscle contractility in the inflamed state.

KW - Acetylcholine

KW - Calcium

KW - Calcium influx

KW - Inflammatory bowel disease

KW - Inositol 1,4,5-trisphosphate

KW - Intracellular calcium stores

KW - Motility

KW - Ryanodine

KW - Signal transduction

KW - Smooth muscle

UR - http://www.scopus.com/inward/record.url?scp=0034016097&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034016097&partnerID=8YFLogxK

M3 - Article

VL - 278

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 2 41-2

ER -