The authors of this article [Sugiura et al., 2000: (http://www.ncbi.nlm.nih.gov/pubmed/10758360)] discuss the capacity of arginine hydrochloride to induce hyperchloremic metabolic acidosis (so-called normal anion gap metabolic acidosis), partly by the excess intake (or infusion, during an intravenous infusion) of chloride and partly, in theory, by the metabolism of arginine per se (this second mechanism is essentially the same as the mechanism discussed in an article I discussed recently, whereby the "activation" of the urea cycle by arginine produces an increase in the consumption of bicarbonate and can reduce plasma bicarbonate). One approach would be to use free-form L-arginine, which is negatively-charged, as opposed to the neutral L-arginine hydrochloride. Usually, the amount of HCl (which would be absorbed as Cl-) provided by hydrochloride salts of medications or other compounds is so small as to have no effect on the plasma anion gap (the plasma sodium concentration, in mEq/L, minus the sum of the plasma concentrations, in mEq/L, of the chloride and bicarbonate anions). [The plasma potassium concentration is sometimes included and added to the plasma sodium concentration, but the plasma potassium concentration is normally low (most potassium is present intracellularly)]. But when a person takes an amino acid as an amine salt, such as in the case of arginine hydrochloride, the intake of chloride can be large and can cause metabolic acidosis that is not reflected in the anion gap (the excess of chloride decreases the anion gap, which would usually be elevated by metabolic acidosis). But, to some extent, Sugiura et al. (2000) are saying that cutting out the excess of chloride might not prevent the acidosis. It's worth noting that some articles have noted the potential for hyperchloremic metabolic acidosis from oral L-arginine hydrochloride, and so the problem may not be confined to situations in which the arginine HCl is infused intravenously (parenterally, such as during total parenteral nutrition) [Soriano, 2002: (http://jasn.asnjournals.org/cgi/reprint/13/8/2160)(http://www.ncbi.nlm.nih.gov/pubmed/12138150?dopt=Abstract)].
Pedrinelli et al. (1995) [Pedrinelli et al., 1995: (http://www.ncbi.nlm.nih.gov/pubmed/7589041)] also found that the infusion of arginine hydrochloride caused acidemia, and both Pedrinelli et al. (1995) and Sugiura et al. (2000) found significant decreases in the urinary anion gap. A decrease in the urinary anion gap is generally thought to be accompanied by an increase in the urinary ammonium concentration [Battle et al., 1988: (http://www.ncbi.nlm.nih.gov/pubmed/3344005)]. Arginine HCl therefore has the potential, according to those articles (and in my opinion), to acidify the urine, by increasing ammonium excretion, and decrease the serum bicarbonate level. In contrast, L-glutamine has sometimes been shown to increase the urinary ammonium level, thereby acidifying the urine, and increase serum bicarbonate (see past postings). In my opinion, this means that taking L-glutamine would not be expected to counteract or balance out the acid-base disturbances that arginine HCl could potentially cause. It might to some extent (to the extent that the effect of arginine occurs via an increase in ureagenesis), but these are the types of things that are worth discussing with one's doctor and being aware of.
Part of the reason these types of things are of interest to me is that the secondary effects of some of these acid-base disturbances can, under some circumstances, in my opinion, lead to elevations (or pathological decreases) in intracranial pressure. The rate of cerebrospinal fluid production can be altered in pathological ways by acid-base dysequilibria between "compartments," such as between the blood and CSF. Carbonic anhydrase inhibitors, for example (inhibitors of enzymes that interconvert bicarbonate and dissolved carbon dioxide gas), such as acetazolamide, are used to reduce CSF production and decrease intracranial pressure, in the context of intracranial hypertension from a variety of causes. Maren and Broder (1970) [Maren and Broder, 1970: (http://www.ncbi.nlm.nih.gov/pubmed/5441150?dopt=Abstract)] found that both chloride and bicarbonate transport from the blood to the CSF can influence the rate of CSF production, and severe disturbances in systemic acid-base balance could, in some people, in my opinion, conceivably lead to intracranial hypertension or hypotension and produce serious complications involving the brainstem, etc. (brainstem herniations can result from intracranial hypotension, and intracranial hypertension can produce serious problems). Also, hypophosphatemia or reductions in the serum ionized calcium (hypercalcemia, more commonly) can accompany increases in the serum bicarbonate level, under some circumstances, and have sometimes been shown to produce intracranial hypertension. It's not my opinion that many or most people would experience any of these effects, even in the presence of a mild acid-base disturbance/dysequilibrium. But it's the type of thing that's worth discussing with one's doctor. The potential for these types of problems to occur in some contexts is, in my opinion, something that is worth taking seriously and being cognizant of.
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