404 HERMAN O. MOSENTHAL 



The impression that hypertension is characteristic of the uremic state 

 (Muller) is not substantiated by observations. A recent case of secondary 

 contracted kidney dying in uremia with a urea nitrogen well over 100 

 mg. per 100 c.c. of blood showed a systolic blood pressure of approximately 

 120 to 130 mm. of mercury and no higher for several weeks before death. 

 This is not an unusual occurrence. The bare fact remains that most clin- 

 icians and investigators interested in blood pressure problems believe that 

 increased vasomotor tone is responsible for the hypertension characteristic 

 of Bright's disease, as well as of those states in which the arterial tension 

 assumes a higher level independently of any renal disease. This is based 

 largely on the very definite evidence that the musculature of the arteries 

 is overactive in these cases and that the blood pressure shows very marked 

 variations on slight provocation. There may be other substances, besides 

 those already considered, which will increase the vasomotor tone and con- 

 sequently be responsible for a rise in blood pressure. These will be taken 

 up under separate headings in the following paragraphs. 



Suprarenal Secretion (Epinephrin). The explanation of hypertension 

 in nephritis that meets all theoretical demands, more perfectly than any 

 other, is the one that attributes increased vascular tone to an excess of 

 epinephrin in the blood. Not only blood pressure changes but also the 

 occurrence of hyperglycemia in Bright's disease may be attributed to this 

 cause. Much time and effort have been spent in bringing positive proof 

 of the overactivity of the suprarenal glands in this connection. Thus 

 far such attempts have been barren of any positive results. Janeway 

 summarized the work of others and his own researches on this subject and 

 came to the conclusion that there was no adequate method to demonstrate 

 epinephrin quantitatively in the blood. Such a state of affairs naturally 

 must leave the problem of the relation of the suprarenal glands to hyper- 

 tension in nephritis an open question, however tempting it may be to as- 

 sume, from a theoretical point of view, that, there is an overproduction of 

 the internal secretion of the suprarenal gland to account for an increase in 

 vascular tone and hypertension. 



The idea that the overactivity of the suprarenal gland is responsible 

 for hypertension was initiated by Neusser and Wiesel who found an in- 

 creased blood pressure in two cases of carcinoma of the adrenal glands. 

 Volhard showed that a similar state of affairs could exist in hyperne- 

 phroma. The French have been particularly enthusiastic in indorsing this 

 theory. Schur and Wiesel injected another element into this matter when 

 they proposed that the retention of the waste products ordinarily excreted 

 by the kidney stimulated the adrenals to increased activity. However, 

 here, as in many other instances in which an accumulation of urea, etc., 

 in the blood is considered in causative relation to augmented blood pres- 

 sure, it must be recognized that there are many patients in whom the blood 

 chemistry shows a marked rise in the urinary excretory products without 



