ArticlePloS one2013
Apelin-13 inhibits large-conductance Ca2+-activated K+ channels in cerebral artery smooth muscle cells via a PI3-kinase dependent mechanism.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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
27 citing papers in PubMed, 43 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- The Impact of the Apelinergic System on the Cardiovascular System.International journal of molecular sciences · 2025Review
- A Metabolically Stable Apelin-13 Analog Acting as a Potent IInternational journal of molecular sciences · 2025Article
- Vascular imbalance in polycystic ovary syndrome: Insights into endothelial dysfunction.PloS one · 2025Article
- Apelin/APJ system: a novel promising target for anti-oxidative stress in stroke.Frontiers in pharmacology · 2024Review
- Intravenous administration of apeling-13 induces a depressor response by releasing an unidentified substance.Biochemical and biophysical research communications · 2023Article
- Loss of IP3R-BKInternational journal of molecular sciences · 2023Article
- Preeclampsia and Obesity-The Preventive Role of Exercise.International journal of environmental research and public health · 2023Review
- Role of G-protein coupled receptors in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- The Role of Apelin-APJ System in Diabetes and Obesity.Frontiers in endocrinology · 2022Review
- The beneficial roles of apelin-13/APJ system in cerebral ischemia: Pathogenesis and therapeutic strategies.Frontiers in pharmacology · 2022Review
- The role of potassium channels on vasorelaxant effects of elabela in rat thoracic aorta.Turk gogus kalp damar cerrahisi dergisi · 2022Article
- Apelin Does Not Impair Coronary Artery Relaxation Mediated by Nitric Oxide-Induced Activation of BKFrontiers in pharmacology · 2021Article
- Apelin inhibits an endothelium-derived hyperpolarizing factor-like pathway in rat cerebral arteries.Peptides · 2020Article
- The Protective Effects and Mechanisms of Apelin/APJ System on Ischemic Stroke: A Promising Therapeutic Target.Frontiers in neurology · 2020Review
- The biological function of ELABELA and APJ signaling in the cardiovascular system and pre-eclampsia.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Review
- APLN promotes hepatocellular carcinoma through activating PI3K/Akt pathway and is a druggable target.Theranostics · 2019Article
- Vascular effects of apelin: Mechanisms and therapeutic potential.Pharmacology & therapeutics · 2018Review
- Calcium- and voltage-gated BK channels in vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2018Review
- Activation of Large Conductance, Calcium-Activated Potassium Channels by Nitric Oxide Mediates Apelin-Induced Relaxation of Isolated Rat Coronary Arteries.The Journal of pharmacology and experimental therapeutics · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Apelin-13 causes vasoconstriction by acting directly on APJ receptors in vascular smooth muscle (VSM) cells; however, the ionic mechanisms underlying this action at the cellular level remain unclear. Large-conductance Ca(2+)-activated K(+) (BKCa) channels in VSM cells are critical regulators of membrane potential and vascular tone. In the present study, we examined the effect of apelin-13 on BK(Ca) channel activity in VSM cells, freshly isolated from rat middle cerebral arteries. In whole-cell patch clamp mode, apelin-13 (0.001-1 μM) caused concentration-dependent inhibition of BK(Ca) in VSM cells. Apelin-13 (0.1 µM) significantly decreased BK(Ca) current density from 71.25 ± 8.14 pA/pF to 44.52 ± 7.10 pA/pF (n=14 cells, P<0.05). This inhibitory effect of apelin-13 was confirmed by single channel recording in cell-attached patches, in which extracellular application of apelin-13 (0.1 µM) decreased the open-state probability (NPo) of BK(Ca) channels in freshly isolated VSM cells. However, in inside-out patches, extracellular application of apelin-13 (0.1 µM) did not alter the NPo of BK(Ca) channels, suggesting that the inhibitory effect of apelin-13 on BKCa is not mediated by a direct action on BK(Ca). In whole cell patches, pretreatment of VSM cells with LY-294002, a PI3-kinase inhibitor, markedly attenuated the apelin-13-induced decrease in BK(Ca current density. In addition, treatment of arteries with apelin-13 (0.1 µM) significantly increased the ratio of phosphorylated-Akt/total Akt, indicating that apelin-13 significantly increases PI3-kinase activity. Taken together, the data suggest that apelin-13 inhibits BK(Ca) channel via a PI3-kinase-dependent signaling pathway in cerebral artery VSM cells, which may contribute to its regulatory action in the control of vascular tone.
Indexed as
Identifiers
What OpenQuestion holds
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.