The Renal Blood Flow 97 



by the arrows in the chart. In some instances the maximal 

 observed blood flow is of the order of magnitude to be ex- 

 pected in the normal kidney, so we may infer that in great 

 measure, at least, the obstruction is functionally reversible. 



During hyperemia the filtration fraction in the hyper- 

 tensive kidney never increases, as would be expected in prin- 

 ciple were the obstruction on the afferent side of the glom- 

 eruli, but it invariably decreases, as shown by the arrows at 

 the bottom of the chart. Again, this fact points to efferent 

 constriction. The fact that the filtration fraction does not 

 fall as low as in the normal kidney may be attributed to sys- 

 temic hypertension or more probably to the presence of im- 

 potent tubules. 



We have examined the effects of hyperemia on glucose- 

 Tm and diodrast-Tm in only a few of these subjects. In most 

 instances the changes are slight and perhaps not beyond the 

 experimental error, and in no instance as yet have we found 

 evidence that hyperemia opens any inactive glomeruli in the 

 hypertensive kidney. However, in one subject (the next to 

 last on the right in the chart) diodrast-Tm was increased 

 during hyperemia to the remarkable extent of 94 per cent, 

 which means that the quantity of tubular tissue reached by 

 blood was increased during hyperemia to this extent. The 

 simultaneous increase in glucose-Tm was only 6 per cent, 

 indicating that the ischemic tissue which was opened to cir- 

 culation by hyperemia was predominantly tubular in nature. 



Summarizing these functional studies, the picture we ob- 

 tain of the hypertensive kidney is that in this disease there 

 is early and progressive loss of tubular function, as revealed 

 by reduction in the tubular excretory mass (diodrast-Tm). 

 The presence and extent of the destructive process is not re- 



