When mice eat more potassium on normal salt, their kidney's salt-handling channels change: one type (NCC) slows down but another (ENaC) speeds up, especially when aldosterone hits about 2701 pg/24h.

When mice eat a lot of salt, their kidney's salt-handling channels (NCC and ENaC) are already low, and adding more potassium doesn't make ENaC any higher.

In mice, when aldosterone hits about 2701 pg/24h (a bit more than normal), the kidney's ENaC channels jump to their highest activity level.

In mice eating normal salt, even though extra potassium slows down one salt-handling channel (NCC), it doesn't lower blood pressure because another channel (ENaC) starts pulling in more salt instead.