Mitochondrial involvement in carbachol-induced intracellular Ca2+ mobilization and contraction in rat gastric smooth muscle

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 muscarin...

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Veröffentlicht in:Life sciences (1973) 2011-11, Vol.89 (21-22), p.757-764
Hauptverfasser: Correa, Roberta M., Lafayette, Simone S.L., Pereira, Gustavo J.S., Hirata, Hanako, Garcez-do-Carmo, Lúcia, Smaili, Soraya S.
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container_end_page 764
container_issue 21-22
container_start_page 757
container_title Life sciences (1973)
container_volume 89
creator Correa, Roberta M.
Lafayette, Simone S.L.
Pereira, Gustavo J.S.
Hirata, Hanako
Garcez-do-Carmo, Lúcia
Smaili, Soraya S.
description 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. 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. Results show that CCh (1μM)-induced contraction was inhibited by FCCP in a concentration-dependent manner. In cultured smooth muscle cells CCh (1μM) 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. 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.
doi_str_mv 10.1016/j.lfs.2011.08.003
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subjects Animals
Calcium
Calcium - metabolism
Calcium Signaling - drug effects
Carbachol
Carbachol - pharmacology
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone - pharmacology
Cells, Cultured
Contraction
dyes
gastric fundus
homeostasis
Immunohistochemistry
In Vitro Techniques
Male
membrane potential
Mitochondria
Mitochondria, Muscle - drug effects
Mitochondria, Muscle - metabolism
mitochondrial membrane
Muscle Contraction - drug effects
Muscle, Smooth - drug effects
Muscle, Smooth - metabolism
myocytes
Myocytes, Smooth Muscle - physiology
Rats
Rats, Wistar
Receptors, Muscarinic - drug effects
Sarcoplasmic Reticulum - drug effects
Sarcoplasmic Reticulum - metabolism
Smooth muscle
Stomach - drug effects
Stomach - metabolism
Uncoupling Agents - pharmacology
title Mitochondrial involvement in carbachol-induced intracellular Ca2+ mobilization and contraction in rat gastric smooth muscle
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