The Renal Response in Man to Acute Experimental Respiratory Alkalosis and Acidosis1

Volhard-Harvey method (9), ammonia by the method of Folin and Bell (10) using a Klett-Summerson photom- eter, phosphate by the method of Lowry and Lopez (11), and titratable acidity by titrating to pH 7.4.The bi- carbonate concentration was calculated from the total CO, content and pH of each urine specimen by use of factors for CO, solubility and pK' in urine as functions of urinary total cation concentration, derived from Send- roy, Seelig, and Van Slyke (12).Methods of blood sampling and analyses were de- scribed in the previous paper (1).CALCULATIONS Urinary electrolytes in microequivalents per minute (i&Eq.per min.)are presented as excretion rates (UV) rather than clearances, thus permitting immediate com- parison of cation-anion equivalents.The cations deter- mined were sodium, potassium, and ammonium; the anions were chloride, bicarbonate, and (in part) phos- phate.Magnitude of acid-base disturbances (A HCO,-e).Un- der conditions termed a "steady state" the rate at which carbon dioxide from cellular metabolism is added to the extracellular fluid equals the rate at which it is lost from the body, and there is no resulting acid-base effect on the extracellular fluid.When the pulmonary component is disturbed, as by hyperventilation or CO2 inhalation, a net quantity of CO, is removed from or added to the extra- cellular fluid.An acid-base effect is exerted by shifting the following relationship toward either the left or right: RENAL RESPONSE TO RESPIRATORY ALKALOSIS AND ACIDOSIS Hyperventilation +1.00 o pH mean &S.p. + 1.63 -0.16 *0.098 *0.251 '.001 ).