Abstract

Experiments were performed in dogs, utilizing cross-circulation techniques, to examine the role of humoral factors in the production of the diminished net renal tubular reabsorption of sodium that is provoked by the expansion of the extracellular fluid volume. When the extracellular fluid volume of one of a pair of dogs (donor) was expanded by the intravenous infusion of isotonic saline, the rate of sodium excretion (U Na V) increased in the nonexpanded animal (recipient) as well as in the donor. Although the increase in U Na V of the recipients was statistically significant, its magnitude was approximately one-fifth of that of the donors. Modified cross-circulation experiments were designed in order to increase the blood flow from the donor dog to the kidneys of the recipient and from the recipient dog to the kidneys of the donor. This modification resulted in a greater increase in U Na V in the recipient and a lesser increase in U Na V in the donor when the donor was infused intravenously with isotonic saline so that the magnitudes of increase in U Na V in donor and recipient were not statistically significantly different. Neither dilution per se of the extracellular fluid of the donor nor passage of time resulted in an increased U Na V in donors and recipients. Expansion of the blood volume of the donors by the infusion of whole blood resulted in an increased U Na V in the donors but not in the recipients. It is concluded that a humoral factor is responsible, at least in part, for the natriuresis that accompanies the intravenous infusion of isotonic saline and that elaboration of the factor is not a consequence solely of either simple dilution of the extracellular fluid or expansion of the blood volume.

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