Abstract

Ammonia is transported into, within, and out of the mammalian kidney largely by passive means; it is suggested that the transport out may be effected exclusively by non-ionic diffusion to equilibrium. The principal objectives of this communication are to present a general kinetic equation which indubitably describes correctly any steady state of renal ammonia balance, to describe by means of a first-order kinetic equation the relations necessarily obtaining between the determinants of renal ammonia balance postulating diffusion equilibrium of NH3 in the kidney, and to indicate how the postulates expressed by the first-order equation can be tested against experiment through implementation of the terms of the equation for any given steady state. In particular, a detailed treatment has been developed for the particular case of ordinary physiological conditions in normal adult man, using a special equation derived from the general quantitative equation with the aid of certain assumptions appropriate to such conditions. The pH and (NH3) of voided urine must generally exceed the urinary values at the papilla as a result of postpapillary increase of urine pH [and hence of urinary (NH3)], caused by delay in dehydrating H2CO3 newly formed in the distal nephron. Application of a reasonable correction for this postpapillary increase of urine pH and (NH3), applied to the data for voided urines of normal adults, accomplishes satisfactory congruence between the theoretical values yielded by the special equation and experimental estimates of the (NH3) of both high-flow papillary urine and of renal cortical tissue water as functions of the pH of high-flow papillary urine. The correction is based on an assumed value for papillary Pco2which cannot be greatly in error in the case of high-flow urines. A larger error would affect similar corrections in the case of low-flow urine, in particular because CO2 reabsorption beyond the papilla probably causes additional postpapillary rise, of appreciable but 1 Supported in part by a research grant (AM-08114) from the National Instituteof Arthritis and Metabolic Diseases. 2 Supported 1962–1963 by a Graduate Traineeship of the National Institute ofArthritis and Metabolic Diseases, and 1965–1966 by a Special Research Fellowship of the U.S. Public Health Service. unknown magnitude, of the pH of such urine. The values of various correction terms will first be known exactly when measurements of the Pco2of the human renal papilla as a function of varying urine flow rate and pH become available. Meantime the general agreement between theoretical and estimated (NH3) of the renal cortex and of the high-flow urines [including the most acid high-flow urine, where (NH3) of voided urine must be so close to that of papillary urine that a correction is hardly required] supports the soundness of the postulates and assumptions on the basis of which the kinetic equations were developed.

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