Liddles syndrome is mutation in ENac channels rendering them with autonomous activity, unregulated by aldosterone. you get suppression of aldosterone levels through negative feedback. its still wasting potassium because of the negative lumen potential from Na reabsorption.
Gain of function in ENac -> increased Na+ reabsorption -> hypertension. Hypertension -> low aldosterone levels.
Increased Na+ reabsorption increases the Na+/K ATPase on the blood side -> increased K+ into the cell -> increased secretion of K+ into the lumen/urine via K+ channel -> hypokalemia