1084 EXCRETION 



tion in the amount of the proteins ingested finally causes a diminution 

 of the body-proteins, which in turn are drawn upon later on to make 

 good the loss in the intake. Quite similarly, any increase in the protein 

 content of the food gives rise to an increase in the nitrogen of the urine. 

 The nitrogen metabolism of the body, however, cannot be estimated 

 precisely unless a comparison is made between the total nitrogen of 

 the urine and the amount of nitrogen ingested, because only when 

 both factors are known is it possible to determine the character of 

 the intermediary processes. 



The most important nitrogenous constituent of urine is urea. 

 Formerly thought to be produced in the kidneys, it is now a well 

 established fact that it arises elsewhere in the body and is brought to 

 these organs in the form of a rather complete precursor. The renal 

 cells, therefore, merely remove this product from the blood by virtue 

 of a peculiar selective power. We know this to be true, because the 

 formation of urea and other waste products of this type continues 

 even after the kidneys have been extirpated or have been rendered 

 functionally useless by disease. This substance then accumulates in 

 the blood and gives rise to the condition of uremia. It should be 

 noted, however, that the poison acting at this time, is not the urea nor 

 any other normal constituent of urine, but some intermediary product 

 of protein catabolism. The question pertaining to the place of origin 

 of this substance seems to have been decided in favor of the liver, 

 because : 



(a) The removal of this organ in mammals proves fatal owing to the accumula- 

 tion of certain catabolic substances. This is indicated by the gradual diminution 

 of the urea content of the urine. A similar effect may be produced by the establish- 

 ment of an Eck fistula, the urea of the urine then being lessened and the ammonia 

 increased. 



(b) The extirpation of the liver in the frog and allied animals brings about a 

 substitution of the urea by ammonia. 



(c) Such diseases as cirrhosis and yellow atrophy of the liver are characterized 

 by a similar change. In the latter case, the amino-acids, such as leucine and 

 tyrosine, appear in the urine, because they escape further reduction in the liver 

 and pass directly into the urine. 



(d) If amino-acids, such as glycine, leucine, arginine, and others are adminis- 

 tered by the mouth or are injected into the blood-stream, the urea excretion is 

 increased. 



This view, that urea is the result of a conversion of the amino-acids 

 by the cells of the liver, is also strengthened by the fact that some of 

 these bodies may be made to undergo this change in the test tube. 

 In the case of arginine, Kossel and Dakin 1 have found that it consists 

 of a urea radicle and a substance known as ornithine. On hydrolysis 

 it splits into urea and ornithine. This same reaction is supposed to 

 occur in the liver under the influence of arginase, the arginine then 

 being split up into simpler compounds which are again combined 



1 Zeitschr. fur Physiol. Chemie, xlii, 1904, 181. 



