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Am J Physiol Gastrointest Liver Physiol 278: G234-G242, 2000;
0193-1857/00 $5.00
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Vol. 278, Issue 2, G234-G242, February 2000

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

Xuan-Zheng Shi and Sushil K. Sarna

Departments of Surgery and Physiology, Medical College of Wisconsin and Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53226

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.

smooth muscle; motility; inflammatory bowel disease; signal transduction; calcium; acetylcholine; calcium influx; intracellular calcium stores; inositol 1,4,5-trisphosphate; ryanodine


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