Well, you sort of have it backwards. It isn't that HCO3- reabsorption causes contraction alkalosis. Instead, ECF volume contraction causes metabolic alkalosis.
1. ECF volume contraction (dehydration from vomiting, for example) stimulates isosmotic reabsorption in the proximal tubule (because the body wants to increase volume) as well as stimulates HCO3 reabsorption; therefore, the volume contraction alone can stimulate HCO3 reabsorption. This is mainly via Starling forces.
2. In addition, when a person is volume contracted (dehydrated) the kidney activates the RAAS system. Angiotensin II stimulates Na/H exchange in the proximal tubule. When this happens, Na enters the proximal tubule cells and H leaves. The Na enters so that water will follow and we can increase blood volume. If the H leaves, it will stimulate HCO3 reabsorption (remember: H + HCO3 = H2CO3 which is then made into H20 and CO2 in the lumen by carbonic anhydrase; the H20 and CO2 diffuse across the proximal tubule cell wall, are converted into H2CO3 by carbonic anhydrase and the H2CO3 will then become H and HCO3; the HCO3 will be transported into the blood and the H will be recycled and used by the Na/H pump to reabsorb another filtered HCO3). Aldosterone also works to stimulate H secretion and thus the reabsorption of filtered HCO3. This phenomenon that I just described is termed contraction alkalosis and literally means a metabolic alkalosis that occurs secondary to ECF volume contraction.
This is an important phenomenon and is especially important in patients who are undergoing aggressive diuretic therapy and can be a complicating factor in patients with a metabolic alkalosis from a multiple day history of vomiting. The diuretics can obviously cause volume contraction which will stimulate the resorptive mechanisms I described above. Vomiting alone will cause a metabolic alkalosis due to the loss of acid from the stomach. If the patient is volume contracted from multiple days of vomiting, as well as not eating or drinking because they obviously can't keep it down and just plain don't feel like it, then this volume contraction will stimulate the RAAS system which, through the mechanism described above, will further complicate a metabolic alkalosis due to vomiting.
I also feel it may be important to include this here, as I think it is a pretty cool phenomenon and can really add to our understanding of acid/base disturbances. In the patient I described who had a multiple day history of vomiting and metabolic alkalosis, this patient can actually have a wide anion gap (if you were to calculate it [and you should calculate it with any acid/base disorder]; and this may be presented to you in a question stem and if you were to see it, you may already be thinking, "Hey, a wide anion gap always means metabolic acidosis!"). This sounds strange, since we are talking about an alkalosis and anion gaps are normally reserved for metabolic acidosis. I mention this because this patient most likely hasn't been eating, and if he/she has, it probably hasn't stayed in their stomach. Therefore, the body has switched to fatty acid beta-oxidation, which produces ketone bodies. These ketone bodies can build up and increase the anion gap. I feel like this is a neat phenomenon because it goes to show that a wide anion gap is not always due to a metabolic acidosis; instead, it can occur with other acid/base disturbances, such as a metabolic alkalosis.
If none of this makes sense, let me know. I find acid/base disturbances particularly interesting. And if anyone finds any of this to be incorrect, let me know as well.
