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Updated: May 29, 2026

In vitro Measurements of Tracheal Constriction Using Mice
Published on: June 25, 2012
Mitochondrial involvement in carbachol-induced intracellular Ca2+ mobilization and contraction in rat gastric smooth
Roberta M Correa1, Simone S L Lafayette, Gustavo J S Pereira
1Department of Pharmacology, Paulista School of Medicine, Federal University of São Paulo (UNIFESP/EPM), Brazil.
Aims:
Mitochondria are important modulators of Ca2+ homeostasis. However, it is not clear if they modulate and participate in smooth muscle signaling and contraction. The aim of the present work was to investigate the role of mitochondria in Ca2+ transients and contraction induced by metabotropic muscarinic receptor activation in rat gastric smooth muscle.
Main Methods:
Carbachol (CCh)-induced contraction was investigated in the absence or presence of increasing concentration of mitochondrial protonophore, carbonyl cyanide p-(trifluoro-methoxy)phenyl-hydrazone (FCCP), in gastric fundus strips. Ca2+ and mitochondrial membrane potential (ΔΨm) measurements were performed in primarily cultured gastric smooth muscle cells loaded with FURA-2 or TMRE dyes.
Key Findings:
Results show that CCh (1 μM)-induced contraction was inhibited by FCCP in a concentration-dependent manner. In cultured smooth muscle cells CCh (1 μM) caused a cytosolic Ca2+ rise. Preincubation with FCCP strongly inhibited CCh-evoked Ca2+ transients indicating that mitochondria shape intracellular Ca2+ signals. CCh induced elevations of ∆Ψm in 60% of the individual mitochondrion analyzed.
Significance:
Taken together our results indicate that CCh induces release of Ca2+ from intracellular stores, which may be modulated by mitochondria. Thus, mitochondria participate of the intracellular Ca2+ homeostasis in muscarinic contraction in gastric fundus smooth muscle.
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