Metabolic alkalosis mimicking the acute sequestration of HCl in rats: bucking the alkaline tide.

Loss or sequestration of HCl induces an acute metabolic alkalosis. The purpose of these experiments was to examine the renal handling of bicarbonate (HCO3-) in awake, euvolemic rats to determine if a significant degree of bicarbonaturia would develop because, if present, it could lead to large negative balances for sodium (Na+) and/or potassium (K+). Metabolic alkalosis was induced acutely by creating the equivalent of an acute and large loss of HCl; the net effect was to lose Cl- and gain equimolar HCO3- in rats that were in Na+ and K+ balance. A loop diuretic induced the loss of 1,860 mumol Na+, 842 mumol K+ and 2,444 mumol Cl- over a 4-h period; the loss of Cl- was replaced as its Na+ or K+ salt by infusing equivalent amounts of NaHCO3 and KHCO3 (ultimately, a "simple exchange" of 2,444 mumol of HCO3- for Cl-). Metabolic alkalosis was sustained for 4 h (mean plasma [HCO3-] = 43 mmol/L); there was a parallel fall in the plasma [Cl-]. From a renal perspective, the fractional excretion of HCO3- was only 0.4%. This adaptation could be viewed as potentially life-saving, because excretion of NaHCO3 would result quickly in a severe reduction in ECF volume and metabolic acidosis and, in addition, in a severe degree of K(+)-depletion.