A B S T R A C T The present studies were designed to characterize sodium transport in the jejunum and ileum of humans with respect to the effects of water flow, sodium concentration, addition of glucose and galactose, and variations in anionic composition of luminal fluid. In the ileum, sodium absorption occurred againstvery steep electrochemical gradients (110 mEq/liter, 5-15 mv), was unaffected by the rate or direction of water flow, and was not stimulated by addition of glucose, galactose, or bicarbonate. These findings led to the conclusion that there is an efficiently active sodium transport across a membrane that is relatively impermeable to sodium. In contrast, jejunal sodium (chloride) absorption can take place against only the modest concentration gradient of 13 mEq/ liter, was dramatically influenced by water movement, and was stimulated by addition of glucose, galactose, and bicarbonate. The stimulatory effect of glucose and galactose was evident even when net water movement was inhibited to zero by mannitol. These observations led to the conclusion that a small fraction of jejunal sodium absorption was mediated by active transport coupled either to active absorption of bicarbonate or active secretion of hydrogen ions. The major part of sodium absorption, i.e. sodium chloride absorption, appeared to be mediated by a process of bulk flow of solution along osmotic pressure gradients. The stimulatory effect of glucose and galactose, even at zero water flow, was explained by a model in

Considerable evidence (1-6) has been adduced to support the hypothesis that the reabsorption of filtered HCO3-by the kidney is mediated by a single mechanism, operative in both the proximal and distal portions of the nephron, which involves the secretion of cellular He in exchange for luminal Na+. The secreted Ho reacts with filtered HC03-to form H2CO3, which then decomposes to C02 and H20.Difficulties arise, however, when the details of the process are examined. In the steady state, the rate at which the H2CO3 is removed from the luminal fluid must equal the rate at which H+ is secreted. Walser and Mudge (7) have estimated that for the uncatalyzed dehydration of H2C03 to account for the observed rates of HC03-reabsorption, the steady-state concentration of H2C03 in luminal fluid must be at least tenfold greater than the concentration that would exist were H2C03 in equilibrium with the C02 tension of luminal fluid and plasma. As a result of the excess H2C03, the steady-state pH would be approximately 1 pH U lower than would be predicted from the luminal concentration of HC03-and the C02 tension of plasma, assuming complete equilibration of luminal H2C03 with plasma C02. A marked disequilibrium pH ' would exist.Two lines of evidence have been advanced to support the presence of a disequilibrium pH in the proximal tubule. Rector and Carter (8) perfused single proximal tubules with NaHCO3 * Submitted for publication July 27, 1964; accepted October 29, 1964. Supported in part by a grant from the American Heart Association and in part by grants 5 TI AM-5028 and 5 TI HE-5469 from the National Institutes of Health.'The difference between the actual pH, under conditions where C02 and H2CO0 are not in equilibrium, and the calculated equilibrium pH will be termed "disequilibrium" pH. and estimated the steady-state intraluminal pH from the change in color of various acid-base indicators. The pH was found to be about 1.5 U lower than the predicted equilibrium pH. However, since the color change could result from loss of dyes by either reabsorption or binding to cell proteins, the validity of these results may be questioned. Bank and Aynedjian (9) measured intratubular pH by aspirating tubular fluid into quinhydrone microelectrodes and comparing the readings while the electrode was still in the tubular lumen with the values obtained when the fluid was removed from the tubule and permitted to reach equilibrium. With this technique, they found the intratubular pH to be 2.0 to 2.5 pH U below the equilibrium pH. These results, however, are open to the serious objection that a disequilibrium pH of this magnitude would require the generation of H2CO3 at a rate 10 to 50 times greater than is theoretically possible, as judged from the rate of HC03-reabsorption.The presence of a disequilibrium pH, however, is not a necessary consequence of the hypothesis that H+ secretion mediates HC03-reabsorption. An equilibrium pH could obtain if H2CO3 were rapidly removed from the tubular urine by either of two mechanisms: 1) nonionic diffusion...

Summary. We used three methods to examine the relationship among intracellular pH, transmembrane potential, and extracellular pH. Singlebarreled electrodes permitted the determination of resting potential and intracellular pH with a minimum of cellular injury. Double-barreled electrodes, which incorporated a reference as well as a pH-sensitive electrode in a single tip, facilitated the direct measurement of intracellular pH without the interposition of the transmembrane potential. Triple-barreled electrodes permitted measurement of intracellular pH during the controlled hyperpolarization or depolarization of the cell membrane.The results of all three methods were in close agreement and disclosed that the H+ activity of intracellular and extracellular fluid is in electrochemical equilibrium at any given transmembrane potential. This implies that the determinants of intracellular pH are the transmembrane potential and the blood pH. The actual pH of the normal resting muscle cell is 5.99, as estimated from the normal transmembrane potential and blood pH, or as determined by direct measurements of intracellular pH.

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A B S T R A C T Previous studies evaluating the mechanism of renal HCO-reabsorption have assumed equilibrium between systemic arterial blood and tubular fluid Pco2. We have recently reported that the Pco2 in proximal and distal tubular fluid as well as the stellate vessel significantly exceeded arterial Pco2 by 25.9 +0.92 mm Hg. The purpose of this study was to determine directly, for the first time, pH, Pco2, and total CO2 concentration in the accessible structures of the rat renal cortex with both microelectrodes and microcalorimetry. In addition, the concentrations of chloride and total CO2 were compared in the stellate vessel. The data demonstrate that: (a) values for total [CO2]