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NEUROREGULATION AND MOTILITY

Changes in guinea pig gallbladder smooth muscle Ca²⁺ homeostasis by acute acalculous cholecystitis

Department of Physiology, Nursing School, University of Extremadura, Caceres, Spain

Submitted 24 June 2005 ; accepted in final form 12 August 2005

Impaired smooth muscle contractility is a hallmark of acute acalculous cholecystitis. Although free cytosolic Ca²⁺ ([Ca²⁺]_i) is a critical step in smooth muscle contraction, possible alterations in Ca²⁺ homeostasis by cholecystitis have not been elucidated. Our aim was to elucidate changes in the Ca²⁺ signaling pathways induced by this gallbladder dysfunction. [Ca²⁺]_i was determined by epifluorescence microscopy in fura 2-loaded isolated gallbladder smooth muscle cells, and isometric tension was recorded from gallbladder muscle strips. F-actin content was quantified by confocal microscopy. Ca²⁺ responses to the inositol trisphosphate (InsP₃) mobilizing agonist CCK and to caffeine, an activator of the ryanodine receptors, were impaired in cholecystitic cells. This impairment was not the result of a decrease in the size of the releasable pool. Inflammation also inhibited Ca²⁺ influx through L-type Ca²⁺ channels and capacitative Ca²⁺ entry induced by depletion of intracellular Ca²⁺ pools. In addition, the pharmacological phenotype of these channels was altered in cholecystitic cells. Inflammation impaired contractility further than Ca²⁺ signal attenuation, which could be related to the decrease in F-actin that was detected in cholecystitic smooth muscle cells. These findings indicate that cholecystitis decreases both Ca²⁺ release and Ca²⁺ influx in gallbladder smooth muscle, but a loss in the sensitivity of the contractile machinery to Ca²⁺ may also be responsible for the impairment in gallbladder contractility.

contractility; calcium stores; calcium channels; F-actin; calcium ion

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