ArticleAmerican journal of physiology. Cell physiology2014
Ethanol-mediated relaxation of guinea pig urinary bladder smooth muscle: involvement of BK and L-type Ca2+ channels.
Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Effects of Solvents, Emulsions, Cosolvents, and Complexions on Ex Vivo Mouse Myometrial Contractility.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Age-dependent decrease in TRPM4 channel expression but not trafficking alters urinary bladder smooth muscle contractility.Physiological reports · 2021Article
- Urinary bladder smooth muscle ion channels: expression, function, and regulation in health and disease.American journal of physiology. Renal physiology · 2020Review
- Urinary incontinence and cardiovascular disease: a narrative review.International urogynecology journal · 2020Review
- TRPM4 channel inhibitors 9-phenanthrol and glibenclamide differentially decrease guinea pig detrusor smooth muscle whole-cell cation currents and phasic contractions.American journal of physiology. Cell physiology · 2020Article
- Preparation and Utilization of Freshly Isolated Human Detrusor Smooth Muscle Cells for Characterization of 9-Phenanthrol-Sensitive Cation Currents.Journal of visualized experiments : JoVE · 2020Article
- Detrusor Smooth Muscle KFrontiers in physiology · 2020Review
- Properties of single-channel and whole cell ClAmerican journal of physiology. Cell physiology · 2019Article
- A biophysically constrained computational model of the action potential of mouse urinary bladder smooth muscle.PloS one · 2018Article
- Testosterone decreases urinary bladder smooth muscle excitability via novel signaling mechanism involving direct activation of the BK channels.American journal of physiology. Renal physiology · 2016Article
- Modulation of BK Channels by Ethanol.International review of neurobiology · 2016Review
- Novel mechanism of hydrogen sulfide-induced guinea pig urinary bladder smooth muscle contraction: role of BK channels and cholinergic neurotransmission.American journal of physiology. Cell physiology · 2015Article
- Article
- Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Review
- Bladder smooth muscle strip contractility as a method to evaluate lower urinary tract pharmacology.Journal of visualized experiments : JoVE · 2014Article
- Ethanol modulation of mammalian BK channels in excitable tissues: molecular targets and their possible contribution to alcohol-induced altered behavior.Frontiers in physiology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mechanisms underlying ethanol (EtOH)-induced detrusor smooth muscle (DSM) relaxation and increased urinary bladder capacity remain unknown. We investigated whether the large conductance Ca(2+)-activated K(+) (BK) channels or L-type voltage-dependent Ca(2+) channels (VDCCs), major regulators of DSM excitability and contractility, are targets for EtOH by patch-clamp electrophysiology (conventional and perforated whole cell and excised patch single channel) and isometric tension recordings using guinea pig DSM cells and isolated tissue strips, respectively. EtOH at 0.3% vol/vol (~50 mM) enhanced whole cell BK currents at +30 mV and above, determined by the selective BK channel blocker paxilline. In excised patches recorded at +40 mV and ~300 nM intracellular Ca(2+) concentration ([Ca(2+)]), EtOH (0.1-0.3%) affected single BK channels (mean conductance ~210 pS and blocked by paxilline) by increasing the open channel probability, number of open channel events, and open dwell-time constants. The amplitude of single BK channel currents and unitary conductance were not altered by EtOH. Conversely, at ~10 μM but not ~2 μM intracellular [Ca(2+)], EtOH (0.3%) decreased the single BK channel activity. EtOH (0.3%) affected transient BK currents (TBKCs) by either increasing frequency or decreasing amplitude, depending on the basal level of TBKC frequency. In isolated DSM strips, EtOH (0.1-1%) reduced the amplitude and muscle force of spontaneous phasic contractions. The EtOH-induced DSM relaxation, except at 1%, was attenuated by paxilline. EtOH (1%) inhibited L-type VDCC currents in DSM cells. In summary, we reveal the involvement of BK channels and L-type VDCCs in mediating EtOH-induced urinary bladder relaxation accommodating alcohol-induced diuresis.
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