100 Physiology of the Kidney 



etiology of hypertension, or at least on the course of renal 

 injury, than can the mere demonstration of the existence of 

 ischemia per se. 



In the ordinary course of events it would be encumbent 

 upon me to relate the above facts to our rapidly expanding 

 knowledge of the pathology of hypertension, and particularly 

 to the demonstration by Goldblatt and his collaborators, and 

 by numerous other investigators, that hypertension can be 

 produced in animals by moderate renal ischemia, and that this 

 hypertension is caused by a substance which is absorbed into 

 the blood from the ischemic renal tissue and which medi- 

 ately or immediately evokes generalized vasoconstriction. 

 This work has, however, been so frequently reviewed that 

 repetition seems superfluous.^'^^'^^'"'^^'^''"^"^ Rather may I be al- 

 lowed to relate this discovery to our own investigations, and, 

 speaking as a physiologist, comment upon the broader im- 

 plications of this problem. 



That the Goldblatt principle plays a primary, causal role 

 in some forms of human hypertension is very definitely in- 

 dicated by the demonstration that all signs of the disease 

 are in some instances obliterated by the removal of a single 

 diseased kidney or by the surgical correction of locally im- 

 paired renal f unction. ^^^^^*^ Consequently the process of ex- 

 cluding known specific pathology of the kidneys in order to 

 arrive at a residual entity which may be called "essential hy- 

 pertension," in that it has no demonstrable renal basis, is per- 

 haps akin to what the biologist calls '*species splitting", and 

 too much ardor in this direction may lead us into as much 

 error as would the careless neglect of specific renal impair- 

 ment (See 23). The present demonstration that hyperten- 

 sive disease, when unaccompanied by specific renal pathology, 



