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Am J Physiol Cell Physiol 273: C1679-C1689, 1997;
0363-6143/97 $5.00
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Vol. 273, Issue 5, C1679-C1689, November 1997

Regulation of intracellular calcium in human esophageal smooth muscles

Stephen M. Sims1, Yang Jiao1, and Harold G. Preiksaitis1,2,3

Departments of 1 Physiology and 2 Medicine, University of Western Ontario, London, Ontario N6A 5C1; and 3 Lawson Research Institute, St. Joseph's Health Centre, London, Ontario, Canada N6A 4V2

We have investigated sources of Ca2+ contributing to excitation of human esophageal smooth muscle, using fura 2 to study cytosolic free Ca2+ concentration ([Ca2+]i) in dispersed cells and contraction of intact muscles. Acetylcholine (ACh) caused an initial peak rise of [Ca2+]i followed by a plateau accompanied by reversible contraction. Removal of extracellular Ca2+ or addition of dihydropyridine Ca2+ channel blockers reduced the plateau phase but did not prevent contraction. Caffeine also caused elevation of [Ca2+]i and blocked responses to ACh. Undershoots of [Ca2+]i were apparent after ACh or caffeine. Blockade of the sarcoplasmic reticular Ca2+-ATPase by cyclopiazonic acid (CPA) reduced the ACh-evoked increase of [Ca2+]i and abolished the undershoot, indicating involvement of Ca2+ stores. When contraction was studied in intact muscles, removal of Ca2+ or addition of nifedipine reduced, but did not abolish, carbachol (CCh)-induced contraction. Elevation of extracellular K+ caused contraction that was inhibited by nifedipine, although CCh still elicited contraction. CPA caused contraction and suppressed the CCh-induced contraction, whereas ryanodine reduced CCh-induced contraction. Our studies provide evidence that muscarinic excitation of human esophagus involves both release of Ca2+ from intracellular stores and influx of Ca2+.

acetylcholine; muscarinic receptors; caffeine; fura 2


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