ArticleThe Journal of biological chemistry2010
Ca2+ sparks act as potent regulators of excitation-contraction coupling in airway smooth muscle.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Integrating GPCR Regulation and Calcium Dynamics in Airway Smooth Muscle Function: A Comprehensive Review.Cells · 2026Review
- Augmented KInternational journal of molecular sciences · 2021Article
- Roles of LRRC26 as an auxiliary γ1-subunit of large-conductance CaAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- Transition From Phasic to Tonic Contractility in Airway Smooth Muscle After Birth: An Experimental and Computational Modeling Study.Journal of engineering and science in medical diagnostics and therapy · 2019Article
- Pathophysiological Role of Caveolae in Hypertension.Frontiers in medicine · 2019Review
- Bitter taste receptors as targets for tocolytics in preterm labor therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- The relative contributions of store-operated and voltage-gated CaThe Journal of physiology · 2017Article
- Distinct Effects of CaInternational journal of biological sciences · 2017Article
- The molecular basis of the genesis of basal tone in internal anal sphincter.Nature communications · 2016Article
- Modulating Ca²⁺ signals: a common theme for TMEM16, Ist2, and TMC.Pflugers Archiv : European journal of physiology · 2016Review
- Activation of Ca(2+) -activated Cl(-) channel ANO1 by localized Ca(2+) signals.The Journal of physiology · 2016Review
- Constitutive PKA activity is essential for maintaining the excitability and contractility in guinea pig urinary bladder smooth muscle: role of the BK channel.American journal of physiology. Cell physiology · 2014Article
- Calcium-activated chloride channels anoctamin 1 and 2 promote murine uterine smooth muscle contractility.American journal of obstetrics and gynecology · 2014Article
- Calcineurin upregulates local Ca(2+) signaling through ryanodine receptor-1 in airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Review
- Bitter tasting compounds dilate airways by inhibiting airway smooth muscle calcium oscillations and calcium sensitivity.British journal of pharmacology · 2014Article
- Functional expression of the TMEM16 family of calcium-activated chloride channels in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- The transmembrane protein 16A Ca(2+)-activated Cl- channel in airway smooth muscle contributes to airway hyperresponsiveness.American journal of respiratory and critical care medicine · 2013Article
- Functional effects of KCNQ K(+) channels in airway smooth muscle.Frontiers in physiology · 2013Article
- The cellular and molecular basis of bitter tastant-induced bronchodilation.PLoS biology · 2013Article
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4 authors.
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Abstract
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+ channels. But in many smooth muscles from a variety of organs, Ca2+ sparks can additionally activate Ca2+-activated Cl(-) channels to generate spontaneous transient inward current (STICs). To date, the physiological roles of Ca2+ sparks in this latter group of smooth muscle remain elusive. Here, we show that in airway smooth muscle, Ca2+ sparks under physiological conditions, activating STOCs and STICs, induce biphasic membrane potential transients (BiMPTs), leading to membrane potential oscillations. Paradoxically, BiMPTs stabilize the membrane potential by clamping it within a negative range and prevent the generation of action potentials. Moreover, blocking either Ca2+ sparks or hyperpolarization components of BiMPTs activates voltage-dependent Ca2+ channels, resulting in an increase in global [Ca2+](i) and cell contraction. Therefore, Ca2+ sparks in smooth muscle presenting both STICs and STOCs act as a stabilizer of membrane potential, and altering the balance can profoundly alter the status of excitability and contractility. These results reveal a novel mechanism underlying the control of excitability and contractility in smooth muscle.
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