In the taste bud, Type I cells carry the epithelial sodium channel (ENaC). These are the cells that turn off Type II bitterness-sensing cells, as noted in a previous post (Friday, February 19, 2016). Not much sodium is required for this effect—in other words a food doesn't have to taste particularly salty to taste less bitter.
The ENaC channel has three sub-units, the proteins SCNN1A, SCNN1B, SCNN1G, shown as alpha, beta, and gamma respectively in the illustration below. Together these subunits form a circular opening in the cell membrane that allows sodium to enter the cell.
Diagram of the ENaC channel in Type I taste bud cells.
Image from Wikipedia.
ENaC is blocked by the drug amiloride. If you take this drug, you lose about 20% of your sensitivity to sodium, so we know that this channel makes a partial contribution to salt taste. The trigeminal "hot" receptor TRPV1 contributes the rest.
Each of the ENaC subunits has several genetic variants. The variants in the alpha and gamma chains apparently don't make a difference in sodium sensitivity. However two changes in the beta protein chain make a difference: for people who carry the variants, salt taste is less intense above threshold.*
By contrast, there is a minor genetic variant in TRPV1 that actually increases sensitivity to sodium concentrations above threshold. TRPV1 is associated with pain when activated by heat, ethanol, or capsaicin, the hot ingredient in chili peppers.
The authors of the study state:
"Future studies should aim to examine the attributes of salt taste at these suprathreshold levels and characterize whether individuals perceive the taste stimuli as aversive or pleasurable or salty or painful."As someone who carries two copies of the more sensitive TRPV1 variant (one from each of my parents), I can assure them that salt can be very painful!
An unanswered question: do people with different variants of ENaC get different degrees of suppression of bitterness with salt?
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