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Ketap
03-14-2012, 09:17 AM
hello..i want to ask : how can diuretics (such as thiazide and furosemide) cause metabolic alkalosis? i 've heard that it is because they loss the chloride too much....i don't really understand this..when they block their site of action, they will deliver high NaCl to the distal tubule and then the aldosterone will reabsorb the Na and the body will loss the potassium in exchange...if the sodium is reabsorbed, than doesn't an equal Chloride should be reabsorbed as well? if it is, so how can the diuretic cause the metabolic alkalosis? or am i wrong about it and they loss more chloride than the sodium?thx u :)

kstarhero
09-26-2012, 08:02 PM
Hi Ketap.

You are probably referring to loop diuretics (e.g. frusemide) and thiazides (hydrochlorothiazide) and not potassium sparing diuretics (e.g. amiloride).
Loop diuretics work by inhibiting the Na+/K+/2Cl- transporter in ascending loop of henle (thick part).

As you state, high NaCL delivery to the distal tubules cause increased Na+ reabsorption. This has the effect of increasing the activity of the Na+/k+ atpase pump on the basolateral side of the cells here. THe exit of increased K+ in these cells will exit via channels into the luminal side, "making up" for that Na+ reabsorption. THis is because the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine.

The net effect is K+ secretion and less Cl- is absorbed (as you say), and hence less water reabsorption. Because the Cl- hangs around in the lumen more, there is increased "electronegativity" in the lumen. Furthermore, there is also H+ secretion, which is moved into the lumen being attracted to the negative charge.

Hence, because of high K+ and H+ secretion, there is metabolic alkalosis.

Thiazides work similarly, except they inhibit Na+/Cl- transporter instead.

I hope this helps :)







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