130 



322 J. A. macwilliam 



It is evident that, whatever chemical agencies may be operative in 

 other ways, in persistent high blood pressures there is a marked inter- 

 ference with regulating nervous mechanisms, rendering them ineffective 

 in keeping down the pressure to anything like the normal levels. 



The question of a compensatory influence of raised blood pressure. 

 Allbutt regarded high pressure as an attempt of the organism to main- 

 tain the equilibrium of the circulation. May the rise of pressure be 

 in some sense compensatory to drive more blood through a vital organ 

 that needs it, e.g., heart muscle or brain or kidney? In the last named 

 the high pressure might conceivably be related to the efforts of the 

 kidneys to excrete concentrated urine, salts or waste products when 

 in excess or when the renal mechanism is inadequate. Possibilities in 

 this direction are suggested by the known existence of the sensitive 

 mechanism by which a defective blood supply to the head promptly 

 sets up a rise in aortic pressure through synergetic changes of increased 

 activity of the vasomotor centre and diminished activity of the vagus 

 centre. A compensatory reaction might conceivably develop in con- 

 nection with other important organs where the blood supply may be 

 defective from narrowing of arterial channels or diminution in the 

 number of capillaries, or where functioning of the tissue — relatively 

 defective from other causes — might be improved by a higher capillary 

 pressure. A compensatory relation was suggested by Bier with refer- 

 ence to the kidney and later by others. The existence of a com- 

 pensatory function may be investigated by artificially lowering the 

 pressures (by vaso-dilators, etc.) in order to find whether functional 

 impairment or disturbances, renal, cardiac, or respiratory result 

 from a reduction of the pressure from an elevated level, which, under 

 the conditions present in these cases, had been favourable to efficiency. 

 A recent investigation on such lines by C. Reid (111) does not lend 

 support to the idea of a compensatory relationship as regards renal 

 efficiency, tested by modern methods, blood urea and non-protein 

 nitrogen being estimated and MacLean's urea concentration test, etc. 

 being employed ; the raised pressures present, associated with a variety 

 of kidney conditions, were lowered by nitrites, venesection, etc. 



As regards the effects of high pressures in causing elongation and 

 tortuosity of arteries, it is obvious that such may result from more than 

 one cause. 1. Impairment of the power of the arterial wall to resist 

 distention may do this, even in the absence of abnormally and per- 

 sistently high pressures, from the frequent or continued existence of 

 a relaxed condition of the arterial muscle, especialh^ in arteries with 



