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A major regulator of blood pressure and volume homeostasis in the kidney is the epithelial sodium channel (ENaC). ENaC is composed of alpha(α)/beta(β)/gamma(γ) or delta(δ)/beta(β)/gamma(γ) subunits. The δ subunit is functional in the guinea pig, but not in routinely used experimental rodent models including rat or mouse, and thus remains the least understood of the four subunits. While the δ subunit is poorly expressed in the human kidney, we recently found that its gene variants are associated with blood pressure and kidney function. The δ subunit is expressed in the human vasculature where it may influence vascular function. Moreover, we recently found that the δ subunit is also expressed human antigen presenting cells (APCs). Our studies indicate that extracellular Na + enters APCs via ENaC leading to inflammation and salt-induced hypertension. In this review, we highlight recent findings on the role of extra-renal ENaC in inflammation, vascular dysfunction, and blood pressure modulation. Targeting extra-renal ENaC may provide new drug therapies for salt-induced hypertension.

Epilepsy is one of the most common, chronic, neurological diseases. The pathology of epilepsy is based on abnormal synchronization of neuronal discharges. Epithelial sodium channels, which are constitutively active, non-voltage-gated, highly selective sodium channels belonging to the epithelial sodium channel/degenerin (ENaC/deg) family, contribute to resting membrane potential modulation and subsequent neuronal excitability by providing a sodium influx pathway. Different from the other three subunits, δ ENaC expression is prominent in the human brain cortex and restricted to neurons. The aim of this study was to investigate the expression pattern of δ ENaC in patients with temporal lobe epilepsy (TLE) and in a pilocarpine-induced rat model of epilepsy. Adopting immunohistochemistry, immunofluorescence, and western blot analysis, we found that δ ENaC was restricted to neurons in the temporal neocortices of TLE patients and the cortices and hippocampus of pilocarpine-induced epilepsy rats, which were similar to the corresponding controls. However, δ ENaC expression was significantly elevated in TLE patients and the pilocarpine-induced epileptic rats. The physiological role, the unchanged localization, and the elevated expression of δ ENaC suggested it could play an important role in epilepsy.