The Renal Blood Flow 95 



creased by systemic hypertension and by arteriolar dilatation. 

 And where part of the renal parenchyma has been destroyed, 

 vascular remnants might persist which, within a certain 

 radius of diffusion, could irrigate the nearby residual func- 

 tional tissue and thus produce to all intents and purposes a 

 hyperemia in that tissue. We would expect such vascular 

 remnants to persist where there were being formed what we 

 have previously called impotent tubules, i.e., tubules which 

 have lost their excretory capacity but which remain con- 

 nected with intact, functioning glomeruli. 



The factors enumerated above would also tend to elevate 

 the filtration rate, except that here we must distinguish be- 

 tween constriction of the afferent and efferent arterioles, 

 which in principle will have opposing effects upon the filtra- 

 tion pressure. 



Now hypotension is clearly ruled out of this problem as 

 a cause of renal ischemia, and we are left with a choice be- 

 tween afferent and efferent arteriolar constriction. Let us 

 take as our assumption the premise that the locus of the con- 

 striction is at the efferent arterioles and see to what extent 

 the facts are consonant with it. Efferent arteriolar constric- 

 tion will lead to renal ischemia, as for example, under the ac- 

 tion of adrenin, but because of the maintained or even in- 

 creased filtration pressure which occurs when the constric- 

 tion is on the far side of the filtering bed, the filtration rate 

 will not decrease in a parallel manner but will tend to be 

 maintained in spite of this ischemia. Offsetting the tendency 

 of the vascular constriction to produce ischemia will be the 

 systemic hypertension which is characteristic of the disease; 

 and, where destruction of renal parenchyma has occurred, 

 vascular remnants persisting around defunct tubules may 



