The Renal Blood Flow 99 



tion, particularly under circulatory stress, but it does not 

 demonstrate that the vasomotor paths are involved in the 

 causation of the ischemia under basal conditions. Under basal 

 conditions the renal vasomotor paths are normally inactive, 

 and the determination of whether or not this is true of the 

 hypertensive kidney must await further examination. 



The evidence clearly indicates the presence in the hyper- 

 tensive kidney of impotent tubules, in addition to the indubi- 

 table tubular fragments and scar tissue which result from the 

 destructive process of the disease. Presumably having a good 

 blood supply, these impotent tubules, along with scar tissue 

 and tubular fragments, afford an opportunity for the absorp- 

 tion into the systemic circulation of physiologically active 

 substances. 



On the question of the extent to which hyperemia will 

 restore circulation to such ischemic tissue as is still capable 

 of functioning we would at this time venture only a tenta- 

 tive opinion. Under otherwise basal conditions, some hyper- 

 tensive subjects have failed to show an increase in tubular ex- 

 cretory mass during hyperemia, while in others an increase 

 occurs, one subject showing an increase of functional paren- 

 chyma of nearly 100 per cent. But in this connection we 

 must ask, How long can tubular tissue tolerate ischemia and 

 yet retain instantaneously reversible, functional capacities? 

 And can we expect to discover ischemic but potentially func- 

 tional tissue in every instance, and particularly in the resting 

 quasi-basal conditions under which these observations have 

 been made? It may be that significant reversible ischemia 

 would be observed only under conditions of circulatory stress 

 (fatigue, exercise, venous inadequacy, etc.) The answer to 

 the two questions posed above may throw more light on the 



