There are several mechanisms by which thiazide diuretics cause hypokalaemia (decreased plasma potassium concentration):

- Increased delivery of sodium to the collecting ducts causes the Na/K exchanger to more actively exchange Na for K resulting in K (and H+) loss.
- Activation of renin-angiotensin-aldosterone system by the diuretic hypovolaemia: body responds to hypovolaemia by opposing diuresis, one effect of which is to produce aldosterone which stimulates the Na/K exchanger, resulting in further loss of potassium. For this reason, ACE inhibitors, which inhibit angiotensin II production and therefore aldosterone activation, are frequently used in combination with thiazides to combat hypokalaemia.
- Flow rate in nephron is increased under diuresis, reducing potassium concentration in the lumen, thus increasing the potassium gradient. Potassium loss through the many potassium channels, such as ROMK. These are not exchangers; they allow facilitated diffusion, so the increased gradient is directly responsible for increased diffusion.

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