9.5 : 抗高血压药物：保钾利尿剂

Liddle syndrome involves hyperactive epithelial sodium channels, enhancing sodium reabsorption and potassium excretion in the nephron.

One of the ways potassium-sparing diuretics work is by blocking the sodium channels, curbing sodium influx, and reducing potassium loss in urine.

The increased sodium concentration in the tubular fluid promotes water excretion, ultimately lowering blood volume and pressure.

In hypertension, overactive kidney β₁ receptors or adrenal glands can elevate aldosterone levels.

Aldosterone binds to cytosolic mineralocorticoid receptors in the kidney. The complex enters the nucleus and overexpresses aldosterone-induced proteins.

This increases sodium transport into and potassium out of the bloodstream, elevating blood volume and pressure.

Potassium-sparing aldosterone antagonist diuretics competitively bind to the receptors, inhibiting active complex formation. This reduces the expression and activity of aldosterone-induced proteins.

The low sodium ion concentration in the blood decreases blood volume without potassium loss.

Thiazide and loop diuretics treat hypertension but may cause hypokalemia. Potassium-sparing diuretics, often combined with these agents, maintain potassium levels while treating hypertension.