96 Physiology of the Kidney 



greatly increase the blood available to the intact tubules and 

 thus produce an apparent hyperemia of the residual func- 

 tional tissue. The hypertensive subject, while usually show- 

 ing a relative ischemia, shows an essentially normal filtration 

 rate; these two facts are therefore consonant with the hy- 

 pothesis of efferent arteriolar spasm. Also contributing to the 

 maintenance of the filtration rate, of course, is such systemic 

 hypertension as exists and, what is perhaps more important, 

 the presence of impotent tubules. The fact that some sub- 

 jects in whom extensive destruction of renal parenchyma has 

 occurred show a relative hyperemia may be attributed to 

 vascular remnants without contradicting the assumption that 

 vascular constriction is the primary perturbation. 



In consequence of the maintenance of filtration rate in 

 the face of decreased plasma flow, the filtration fraction is 

 substantially increased. In not a single hypertensive subject 

 examined by us has the filtration fraction been down to the 

 normal value. If the vascoconstriction responsible for the 

 ischemia were on the afferent side of the glomeruli, one would 

 expect to find the filtration fraction below normal in some 

 instances at least, particularly those where the renal paren- 

 chyma is only slightly injured. Failure to do so is strong evi- 

 dence of efferent spasm. 



We may next inquire, is this efferent spasm amenable to 

 physiological reversal, or does it have the nature of a rigid, 

 irreversible occlusion? Information can be obtained on this 

 question by observing the response during the pyrexial re- 

 action, which in the normal kidney produces a substantial 

 hyperemia. Not all subjects studied by us have been ex- 

 amined in this manner, but those who have been examined 

 have invariably shown a hyperemia of some degree, as shown 



