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Activation of the Epithelial Sodium Channel (ENaC) by Serine Proteases
- Source :
- Annual Review of Physiology. 71:361-379
- Publication Year :
- 2009
- Publisher :
- Annual Reviews, 2009.
-
Abstract
- The study of human monogenic diseases [pseudohypoaldosteronism type 1 (PHA-1) and Liddle's syndrome] as well as mouse models mimicking the salt-losing syndrome (PHA-1) or salt-sensitive hypertension (Liddle's syndrome) have established the epithelial sodium channel ENaC as a limiting factor in vivo in the control of ionic composition of the extracellular fluid, regulation of blood volume and blood pressure, lung alveolar clearance, and airway mucociliary clearance. In this review, we discuss more specifically the activation of ENaC by serine proteases. Recent in vitro and in vivo experiments indicate that membrane-bound serine proteases are of critical importance in the activation of ENaC in different organs, such as the kidney, the lung, or the cochlea. Progress in understanding the basic mechanism of proteolytic activation of ENaC is accelerating, but uncertainty about the most fundamental aspects persists, leaving numerous still-unanswered questions.
- Subjects :
- Epithelial sodium channel
medicine.medical_specialty
Proteases
Physiology
Mucociliary clearance
Serpin
Kidney
Serine
Internal medicine
medicine
Animals
Humans
Epithelial Sodium Channels
Lung
Chemistry
Serine Endopeptidases
Pseudohypoaldosteronism
Extracellular Fluid
respiratory system
medicine.disease
Cochlea
Cell biology
medicine.anatomical_structure
Endocrinology
Renal physiology
Subjects
Details
- ISSN :
- 15451585 and 00664278
- Volume :
- 71
- Database :
- OpenAIRE
- Journal :
- Annual Review of Physiology
- Accession number :
- edsair.doi.dedup.....204883daa5d851f0d7ec4f554519a74e