Intracellular calcium was involved in muscarinic currents increased by hypoosmotic membrane stretch in gastric myocytes of guinea pig.
Abstract
AIM: To investigate the role of intracellular calcium in muscarinic currents
increased by hypoosmotic membrane stretch in gastric antral circular myocytes of
the guinea pig.
METHODS: The whole cell patch-clamp technique was used, and the myocytes were
isolated by collagenase. Cells were swelled by hypoosmotic solution (200
Osmmol/kg).
RESULTS: The hypoosmotic membrane stretch markedly increased carbachol-induced
muscarinic currents (ICCh). The ICCh and the increase of ICCh were completely
blocked by quinidine 3 micromol/L, a specific muscarinic current blocker. In
external calcium-free solution hypoosmotic membrane stretch could not increase
ICCh, but in the presence of nicadipine 5 micromol/L, a L-type calcium channel
blocker or gadolinium chloride 100 nmol/L, a stretch-activated cation channel
blocker, the ICCh was still increased by hypoosmotic membrane stretch. When both
nicardipine and gadolinium chloride were added into external solution, ICCh were
not increased by hypoosmotic membrane stretch any more. Ryanodine, a
calcium-induced calcium release (CICR) agonist completely blocked hypoosmotic
membrane stretch-induced increase of ICCh.
CONCLUSION: Hypoosmotic membrane stretch increased ICCh and the increment was
related to influx of external calcium and CICR.
Keywords:
increased by hypoosmotic membrane stretch in gastric antral circular myocytes of
the guinea pig.
METHODS: The whole cell patch-clamp technique was used, and the myocytes were
isolated by collagenase. Cells were swelled by hypoosmotic solution (200
Osmmol/kg).
RESULTS: The hypoosmotic membrane stretch markedly increased carbachol-induced
muscarinic currents (ICCh). The ICCh and the increase of ICCh were completely
blocked by quinidine 3 micromol/L, a specific muscarinic current blocker. In
external calcium-free solution hypoosmotic membrane stretch could not increase
ICCh, but in the presence of nicadipine 5 micromol/L, a L-type calcium channel
blocker or gadolinium chloride 100 nmol/L, a stretch-activated cation channel
blocker, the ICCh was still increased by hypoosmotic membrane stretch. When both
nicardipine and gadolinium chloride were added into external solution, ICCh were
not increased by hypoosmotic membrane stretch any more. Ryanodine, a
calcium-induced calcium release (CICR) agonist completely blocked hypoosmotic
membrane stretch-induced increase of ICCh.
CONCLUSION: Hypoosmotic membrane stretch increased ICCh and the increment was
related to influx of external calcium and CICR.