ReviewPflugers Archiv : European journal of physiology2015
Role of K₂p channels in stimulus-secretion coupling.
Review in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Acute Hypoxia Inhibits KActa physiologica (Oxford, England) · 2026Article
- KArchiv der Pharmazie · 2026Review
- K2P channels as emerging therapeutic targets for pain: insights from functional studies and transcriptomic analyses.Frontiers in pharmacology · 2026Review
- The cornea-trigeminal axis: potassium channels as master regulators of ocular surface homeostasis and sensory transduction.Frontiers in cell and developmental biology · 2026Review
- Co-Expression of TWIK-Related Acid-Sensitive KBiomedicines · 2025Article
- A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ.The Journal of physiology · 2021Article
- Current Drug Treatment Strategies for Atrial Fibrillation and TASK-1 Inhibition as an Emerging Novel Therapy Option.Frontiers in pharmacology · 2021Review
- Pharmacologic TWIK-Related Acid-Sensitive K+ Channel (TASK-1) Potassium Channel Inhibitor A293 Facilitates Acute Cardioversion of Paroxysmal Atrial Fibrillation in a Porcine Large Animal Model.Journal of the American Heart Association · 2020Article
- Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease.Comprehensive Physiology · 2019Article
- Hypoxia-regulated catecholamine secretion in chromaffin cells.Cell and tissue research · 2018Review
- Sortilin in Glucose Homeostasis: From Accessory Protein to Key Player?Frontiers in pharmacology · 2018Review
- Hyperoxia treatment of TREK-1/TREK-2/TRAAK-deficient mice is associated with a reduction in surfactant proteins.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Purinergic signalling mediates bidirectional crosstalk between chemoreceptor type I and glial-like type II cells of the rat carotid body.The Journal of physiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Two-pore domain K(+) (K2P) channels are involved in a variety of physiological processes by virtue of their high basal activity and sensitivity to various biological stimuli. One of these processes is secretion of hormones and transmitters in response to stimuli such as hypoxia, acidosis, and receptor agonists. The rise in intracellular [Ca(2+)] ([Ca(2+)]i) that is critical for the secretory event can be achieved by several mechanisms: (a) inhibition of resting (background) K(+) channels, (b) activation of Na(+)/Ca(2+)-permeable channels, and (c) release of Ca(2+) from intracellular stores. Here, we discuss the role of TASK and TREK in stimulus-secretion mechanisms in carotid body chemoreceptor cells and adrenal medullary/cortical cells. Studies show that stimuli such as hypoxia and acidosis cause cell depolarization and transmitter/hormone secretion by inhibition of TASK or TREK. Subsequent elevation of [Ca(2+)]i produced by opening of voltage-dependent Ca(2+) channels then activates a Na(+)-permeable cation channel, presumably to help sustain the depolarization and [Ca(2+)]i. Agonists such as angiotensin II may elevate [Ca(2+)]i via multiple mechanisms involving both inhibition of TASK/TREK and Ca(2+) release from internal stores to cause aldosterone secretion. Thus, inhibition of resting (background) K(+) channels and subsequent activation of voltage-gated Ca(2+) channels and Na(+)-permeable non-selective cation channels may be a common ionic mechanism that lead to hormone and transmitter secretion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.