Ronghua Zhuge

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Bronchodilators are a standard medicine for treating airway obstructive diseases, and β2 adrenergic receptor agonists have been the most commonly used bronchodilators since their discovery. Strikingly, activation of G-protein-coupled bitter taste receptors (TAS2Rs) in airway smooth muscle (ASM) causes a stronger bronchodilation in vitro and in vivo than β2(More)
1. Local changes in cytosolic [Ca2+] were imaged with a wide-field, high-speed, digital imaging system while membrane currents were simultaneously recorded using whole-cell, perforated patch recording in freshly dissociated guinea-pig tracheal myocytes. 2. Depending on membrane potential, Ca2+ sparks triggered 'spontaneous' transient inward currents(More)
Ca(2+) sparks are highly localized cytosolic Ca(2+) transients caused by a release of Ca(2+) from the sarcoplasmic reticulum via ryanodine receptors (RyRs); they are the elementary events underlying global changes in Ca(2+) in skeletal and cardiac muscle. In smooth muscle and some neurons, Ca(2+) sparks activate large conductance Ca(2+)-activated K(+)(More)
Ca(2+) sparks are small, localized cytosolic Ca(2+) transients due to Ca(2+) release from sarcoplasmic reticulum through ryanodine receptors. In smooth muscle, Ca(2+) sparks activate large conductance Ca(2+)-activated K(+) channels (BK channels) in the spark microdomain, thus generating spontaneous transient outward currents (STOCs). The purpose of the(More)
RATIONALE Asthma is a chronic inflammatory disorder with a characteristic of airway hyperresponsiveness (AHR). Ca(2+)-activated Cl(-) [Cl((Ca))] channels are inferred to be involved in AHR, yet their molecular nature and the cell type they act within to mediate this response remain unknown. OBJECTIVES Transmembrane protein 16A (TMEM16A) and TMEM16B are(More)
Ca 2 sparks are small, localized cytosolic Ca 2 transients due to Ca 2 release from sarcoplasmic reticulum through ryanodine receptors. In smooth muscle, Ca 2 sparks activate large conductance Ca 2 -activated K channels (BK channels) in the spark microdomain, thus generating spontaneous transient outward currents (STOCs). The purpose of the present study is(More)
Ca2+ stores were studied in a preparation of freshly dissociated terminals from hypothalamic magnocellular neurons. Depolarization from a holding level of -80 mV in the absence of extracellular Ca2+ elicited Ca2+ release from intraterminal stores, a ryanodine-sensitive process designated as voltage-induced Ca2+ release (VICaR). The release took one of two(More)
Localized, transient elevations in cytosolic Ca 2 1 , known as Ca 2 1 sparks, caused by Ca 2 1 release from sarcoplasmic reticulum, are thought to trigger the opening of large conductance Ca 2 1 -activated potassium channels in the plasma membrane resulting in spontaneous transient outward currents (STOCs) in smooth muscle cells. But the precise(More)
Ca 2 1 sparks are highly localized cytosolic Ca 2 1 transients caused by a release of Ca 2 1 from the sarcoplasmic reticulum via ryanodine receptors (RyRs); they are the elementary events underlying global changes in Ca 2 1 in skeletal and cardiac muscle. In smooth muscle and some neurons, Ca 2 1 sparks activate large conductance Ca 2 1 -activated K 1(More)
Ca2+ sparks are short lived and localized Ca2+ transients resulting from the opening of ryanodine receptors in sarcoplasmic reticulum. These events relax certain types of smooth muscle by activating big conductance Ca2+-activated K+ channels to produce spontaneous transient outward currents (STOCs) and the resultant closure of voltage-dependent Ca2+(More)