ArticleAmerican journal of hypertension2021
Expression of Exogenous Epithelial Sodium Channel Beta Subunit in the Mouse Middle Cerebral Artery Increases Pressure-Induced Constriction.
Article in American journal of hypertension, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanobiological insight into brain diseases based on mechanosensitive channels: Common mechanisms and clinical potential.CNS neuroscience & therapeutics · 2024Review
- The Epithelial Sodium Channel-An Underestimated Drug Target.International journal of molecular sciences · 2023Review
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Is there a role of proinflammatory cytokines on degenerin-mediated cerebrovascular function in preeclampsia?Physiological reports · 2022Review
- βENaC and ASIC2 associate in VSMCs to mediate pressure-induced constriction in the renal afferent arteriole.American journal of physiology. Renal physiology · 2022Article
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4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPressure-induced constriction (PIC) is inherent to small arteries and arterioles, in which intraluminal pressure-induced vascular smooth muscle cell stretch elicits vasoconstriction. Degenerin (Deg) proteins, such as beta-epithelial Na+ channel (βENaC), have been studied in the PIC response because they are evolutionarily linked to known mechanosensors. While loss of Deg function phenotypes are plentiful, a gain-of-function phenotype has not been studied. The aim of this study was to determine if expression of exogenous βENaC in the isolated middle cerebral artery (MCA) enhances the PIC response.
methodsIsolated MCA segments from female mice (24 weeks, n = 5) were transfected with enhanced green fluorescent protein-βENaC (EGFP-βENaC) or with EGFP alone, incubated overnight at 37 °C, then studied in a pressure myograph.
resultsMechanical/morphological properties and vasoconstrictor responses to KCl and phenylephrine were identical in EGFP-βENaC and EGFP MCAs. In contrast, PIC responses were greater in EGFP-βENaC segments with ~2-fold greater peak myogenic tone.
conclusionsThese data confirm previous findings that βENaC is critical in the PIC response. These data provide proof-of-concept that upregulating βENaC can enhance PIC responses and lay the foundation to test the hypothesis that inflammation-mediated downregulation of βENaC contributes to cerebrovascular dysfunction.
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