American journal of hypertension · 2021
Expression of Exogenous Epithelial Sodium Channel Beta Subunit in the Mouse Middle Cerebral Artery Increases Pressure-Induced Constriction.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Nemeth Zoltan, Ryan Michael J, Granger Joey P, Drummond Heather A
Аннотация
BACKGROUND: Pressure-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.
METHODS: Isolated 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.
RESULTS: Mechanical/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.
CONCLUSIONS: These 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.
METHODS: Isolated 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.
RESULTS: Mechanical/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.
CONCLUSIONS: These 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.