METABOLISM IN NEPHRITIS 403 



Increased Vasomotor Tone. That an increased tonicity of the per- 

 ipheral vessels will result in a rise of blood pressure, provided the heart's 

 force and the blood volume remain constant, requires no proof. Such a 

 change in function, frequently spoken of as "spasm of the peripheral ves- 

 sels/' is generally conceded to be the most likely explanation of the occur- 

 rence of an increased arterial pressure. In a measure, this theory can 

 not be considered to answer the problem completely for it still remains to 

 be determined what the agent or agents are that influence the blood ves- 

 sels in this way, and furthermore it does not satisfy the query as to where 

 the stimulation occurs, in the nervous system or in the walls of the arteries 

 themselves; it is important to be thoroughly informed regarding both of 

 these points before the problem may be considered even as approaching a 

 solution. 



Gull and Sutton originally advanced the idea that an organic lesion 

 which narrowed the lumen of the smaller arteries was the cause of hyper- 

 tension. Such a pathological process will in all probability result in an 

 increased arterial pressure. However, this state of affairs is a rare ex- 

 ception and not the rule, for the smaller blood vessels in hypertensive 

 states maintain their ability to contract and dilate much as in normal in- 

 dividuals. This has been demonstrated by the good reaction such patients 

 exhibit to the vasodilators (Janeway, Matthew, J. Miller, Wallace and 

 Ringer), by the remarkable drop of the hypertension (often 50 mm. of 

 mercury) with rest, even over a period of only a few minutes and a cor- 

 responding rise on excitement, as shown by a number of observers (Hensen, 

 Israel and others) and recently brought out by Boas and by O'Hare, and 

 by the occurrence of sudden extreme elevations of blood pressure, termed 

 "Gefasskrisen" by Pal. 



It was at one time believed that if a part or all of the renal circula- 

 tion were shut off that hypertension would result because of a compensatory 

 effort on the part of the body to effect renal secretion. However fascinat- 

 ing this may be in theory, it is not borne out by the facts in the case; 

 complete extirpation of the kidneys, or ligation of both renal arteries does 

 not result in an increase in the blood pressure; partial occlusion of the 

 renal circulation was supposed by some to bring this about (Katzenstein) 

 but a repetition of these experiments has failed to substantiate the original 

 observation (Alwens, Senator(Z) ). It may be worth noting again that the 

 most frequent and marked instances of hypertension occur when there is 

 no involvement of the kidney whatsoever. Another idea advanced in this 

 connection is that fathered by Johnson who believed that the retention of 

 renal excretory products was the cause of the increased vascular spasm. 

 As far as this hypothesis can be judged, by means of the non-protein nitro- 

 genous constituents of the blood as a criterion, it is incorrect since the 

 arterial pressure in any case apparently remains unchanged whether the 

 blood urea is markedly increased or drops to normal (Mosenthal(/) ). 



