The emerging epithelial Na channel/degenerin family of sodium channels
is rapidly expanding, in particular with new members expressed in mam
malian neurons and potentially involved in pain transmission. Experime
ntal evidence supports a four-subunit stoichiometry for these channels
(although this is still controversial), and basic functional elements
(pore and selectivity filter, amiloride binding site, gating) have st
arted to be attributed to specific domains of the protein. Although mu
ch remains to be done, in the past year progress has been made in the
understanding of several regulatory mechanisms: the control of epithel
ial Na channel translation by mineralocorticoid hormones, the role of
endocytosis and ubiquitination for degradation in the control of the c
hannel density and the role of extracellular proteases.