ArticleBritish journal of pharmacology2010
Compromised vascular endothelial cell SK(Ca) activity: a fundamental aspect of hypertension?
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Differential modulation of SK channel subtypes by phosphorylation.Cell calcium · 2021Article
- Mesenteric arterial dysfunction in the UC Davis Type 2 Diabetes Mellitus rat model is dependent on pre-diabetic versus diabetic status and is sexually dimorphic.European journal of pharmacology · 2020Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Preserved regulation of renal perfusion pressure by small and intermediate conductance KCa channels in hypertensive mice with or without renal failure.Pflugers Archiv : European journal of physiology · 2015Article
- Berberine protects vascular endothelial cells in hypertensive rats.International journal of clinical and experimental medicine · 2015Article
- Selective phosphorylation modulates the PIP2 sensitivity of the CaM-SK channel complex.Nature chemical biology · 2014Article
- Targeting the Small- and Intermediate-Conductance Ca-Activated Potassium Channels: The Drug-Binding Pocket at the Channel/Calmodulin Interface.Neuro-Signals · 2014Review
- Unstructured to structured transition of an intrinsically disordered protein peptide in coupling Ca²⁺-sensing and SK channel activation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Identification of the functional binding pocket for compounds targeting small-conductance Ca²⁺-activated potassium channels.Nature communications · 2012Article
- The vascular endothelium: still amazing us 30 years on.British journal of pharmacology · 2011Article
- Comment from the Editor-in-Chief on correspondence in this issue on immuno-techniques.British journal of pharmacology · 2011Article
- 'Altered' mesenteric artery SK(Ca) : functional implications?British journal of pharmacology · 2011Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Smooth muscle hyperpolarization originating in the endothelium and commonly referred to as the EDHF (endothelium-derived hyperpolarizing factor) response provides a very significant drive to vasodilatation particularly in small resistance arteries. Together with other endothelium-dependent dilator pathways 'EDHF' hyperpolarization is compromised by cardiovascular disease, including hypertension. However, although attenuated vascular hyperpolarization has been described in animal models of hypertension, the underlying mechanisms are not fully understood. In the current issue of the British Journal of Pharmacology, Weston et al. combine classic pharmacological approaches with electrophysiological and molecular techniques to suggest that attenuated endothelium-dependent hyperpolarization (and as a consequence vasodilatation) reflects major disruption of pathways associated with the activation of endothelial small conductance Ca(2+)-activated K-channels (SK(Ca)) in mesenteric arteries from spontaneously hypertensive rats. In addition to reductions in SK(Ca) and K(IR) proteins, changes in caveolin-1 isomers were also detected, possibly indicating channel realignment within plasmalemmal structures.
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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.