The Excretion of Administered Sodium Chloride by the Conscious Dog, and the Effect of Occlusion of the Carotid Arteries

The excretion of sodium chloride administered by stomach tube to the conscious dog was not altered by previous denervation of the kidneys or by injections of desoxycorticosterone acetate. 2. The excretion of administered sodium chloride was not determined by changes in the sodium or chloride concentration of the plasma, but there was a close relationship between the rate of excretion of sodium and total solid content of the plasma, which was used to follow changes in the plasma protein concentration. Ingestion of ammonium chloride or water caused no increase in sodium excretion, and there was no large fall in plasma solid. Ingestion of sodium bicarbonate caused an increased excretion of sodium associated with dilution of the plasma solids, but there was no corresponding increase in the excretion of chloride. 3. Occlusion of both carotid arteries caused immediately an increased output of urine and of both sodium and chloride. This persisted after denervation of the kidneys, and was attributed to the increased arterial pressure produced by the occlusion. 4. The relationship between plasma solid content and rate of excretion of sodium has been plotted, and from this an estimate made of the probable relationship between plasma protein concentration, glomerular filtration rate and sodium excretion. The effects of dilution of plasma protein and of increased arterial blood pressure in increasing sodium excretion have been compared quantitatively. 5. Measurements of inulin or creatinine clearance are not sufficiently accurate to elucidate problems of sodium excretion. 6. The relationship between plasma solid content and rate of excretion of sodium is discussed with reference to the sodium balance of the body.