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.

When mice eat a lot of salt, adding a moderate amount of potassium lowers their blood pressure, showing that potassium's main benefit might be fighting high blood pressure caused by salt.

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.

Even though high potassium lowers a kidney transporter in mice, this doesn't explain the blood pressure changes, suggesting other mechanisms are at play.

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.

In mice eating normal salt, too much potassium (over 1.75% of their diet) makes their blood pressure go up during active hours, especially at high potassium levels like 5%, because of increased activity of certain kidney channels.