Key result
Spontaneous release of Ca2+ from the sarcoplasmic reticulum activates Ca2+-activated Cl- current, contributing to resting membrane potential and mediating nitrergic slow inhibitory junction potentials.
Population
Opossum lower esophageal sphincter (LES) circular smooth muscle (n=25)
Comparison
Pharmacological agents (ODQ, caffeine… vs Baseline/control conditions
Design
Preclinical
Authors
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Supports LES electrophysiology research in models; leaves open translation to human nitrergic signaling or motility disorders.
Spontaneous Ca2+ release from the sarcoplasmic reticulum activates ICl(Ca) to maintain resting membrane potential in opossum LES, and its inhibition underlies nitrergic slow inhibitory junction potentials.
Zhang et al. (2003) studied Opossum lower esophageal sphincter physiology. Pharmacological inhibitors (ODQ, caffeine, ryanodine, cyclopiazonic acid) was evaluated on Resting membrane potential and slow inhibitory junction potentials (sIJPs). Spontaneous release of Ca2+ from the sarcoplasmic reticulum activates Ca2+-activated Cl- current, contributing to resting membrane potential and mediating nitrergic slow inhibitory junction potentials.
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