In mice, more potassium leads to more aldosterone in a straight-line way, but blood pressure rises sharply only when aldosterone hits a certain level (around 4040 pg/24h), then levels off.

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.

When mice eat a lot of salt, adding a moderate amount of potassium lowers their blood pressure by about 3.6 mmHg compared to eating the same high salt without extra potassium.

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.

Long-term high potassium intake in mice leads to higher levels of a hormone called aldosterone in both blood and urine.

Mice missing the AMPKα1 gene produce more aldosterone in their urine and have lower blood pressure than normal mice.