86 Physiology of the Kidney 



and we suspect that it is this cardiac inhibition, presumably 

 mediated through the vagus, which is immediately responsible 

 for cerebral anoxia and loss of consciousness. The importance 

 of cardiac inhibition in syncope has been pointed out by Sir 

 Thomas Lewis,^^ but it has not received the attention which 

 I believe it merits. 



Returning to the kidney, I particularly call your atten- 

 tion to the fact that the subject of the above experiment had 

 essential hypertension. I have exhibited a hypertensive sub- 

 ject rather than a normal one for deliberate reasons. Normal 

 and hypertensive subjects behave very much alike; individu- 

 als in both groups show differences in sensitivity to venous 

 failure, which makes it difficult to quantitate the local renal 

 response. It is enough for the moment to be able to assert 

 that when either the normal or the hypertensive subject as- 

 sumes the upright, immobile posture the blood flow through 

 the kidneys may be substantially reduced by reflex vasocon- 

 striction. 



Let us turn now to the question of what happens in the 

 renal circulation during ischemia and hyperemia. The con- 

 ventionally accepted description for the normal kidney is 

 that essentially all the tubular capillaries are supplied from 

 the efferent glomerular arterioles. If such is the case, con- 

 striction of either afferent or efferent arterioles would be ex- 

 pected to produce some tubular ischemia, even though the 

 glomerular circulation were not completely arrested. But in 

 the pathological kidney, according to Oliver,^^ direct connec- 

 tions exist between the arteriolar tree and the peritubular 

 capillaries; functionally equivalent connections have been 

 described in the normal kidney by Fuchs and Popper,^ and 

 Spanner^^ asserts that in the normal kidney there are numer- 



