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 don't get enough potassium, their kidney transporter becomes more active and blood pressure rises, but a common blood pressure drug can lower it again.

Whether mice get extra potassium for a few days or weeks, a key kidney transporter becomes less active.

Long-term high potassium makes a kidney channel more active, and blocking that channel with a drug lowers blood pressure in mice.

For a few days, extra potassium lowers mice's blood pressure, but after three weeks, it starts to raise it again.

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.