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Smooth Muscle βENaC Deletion Induces Moderate Hypertension and Renal Injury
Tawhida Islam1, Zoltan Nemeth1, Seth Lirette2
1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Kidney360
|July 24, 2026
Summary
Vascular smooth muscle betaENaC is crucial for pressure-induced constriction in renal arteries, protecting against injury. Its absence leads to elevated blood pressure and renal damage in mice.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Molecular Biology
Background:
- Pressure-induced constriction (PIC) of renal vasculature may prevent glomerular barotrauma.
- Degenerin proteins, including beta subunit of the Epithelial Na+ Channel (βENaC), are implicated in PIC.
- Previous research suggests βENaC's role in mediating PIC.
Purpose of the Study:
- To investigate the role of smooth muscle βENaC in renal vascular response.
- To determine the contribution of smooth muscle βENaC to pressure-induced constriction (PIC).
- To assess the impact of smooth muscle βENaC deletion on renal injury and inflammation.
Main Methods:
- Generated smooth muscle βENaC knockout mice (SMC-βENaC-/-).
- Assessed renal interlobar vascular reactivity using myography.
- Evaluated renal inflammation, injury, and blood pressure via histology, blotting, ELISA, flow cytometry, and plethysmography.
Main Results:
- PIC responses were abolished in SMC-βENaC-/- mice.
- Sustained higher systolic blood pressure was observed in SMC-βENaC-/- mice.
- Mild glomerular injury and increased leukocyte infiltration were noted in SMC-βENaC-/- mice.
Conclusions:
- Vascular smooth muscle cell (VSMC) βENaC is essential for PIC in renal vessels.
- PIC, mediated by VSMC βENaC, plays a protective role against renal vascular injury.
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