98 Physiology of the Kidney 



vealed, at least in the milder forms of hypertension, by any 

 reduction in the rate of glomerular filtration, which is main- 

 tained for possibly three reasons, efferent arteriolar constric- 

 tion, the formation of impotent tubules and systemic hyper- 

 tension. There is invariably an ischemia, in terms of absolute 

 blood flow; and usually there is a relative ischemia of the 

 residual functional tissue, though the presence of vascular 

 remnants and perhaps the effect of systemic hypertension 

 may in some instances have the effect of producing a relative 

 hyperemia of the residual functional tissue. 



The frequency with which ischemia relative to the resi- 

 dual functional tissue occurs in these subjects suggests that 

 there exists a perturbation of vascular function which is pri- 

 mary in time and causality to the destruction of renal par- 

 enchyma, i.e., that the destruction of renal parenchyma is a 

 result rather than a cause of the ischemia. The major facts 

 can be explained on the assumption that the immediate per- 

 turbation of function is an excessive constriction of the effer- 

 ent glomerular arterioles, which is in great measure at least 

 functionally reversible under conditions which produce hy- 

 peremia in the normal kidney. The cause of this constriction 

 is, however, undetermined ; it may be due simply to the pres- 

 ence in the systemic circulation of a vasoconstrictor principle 

 which is acting upon the arterioles of the body generally, or 

 it may be a physiological response secondary to occlusion on 

 the afferent side of the glomeruli. 



Neurogenic vasoconstrictor activity, which is elicited by 

 the sustained upright posture and which can produce ischemia 

 in the normal kidney, can aggravate the existant ischemia of 

 the hypertensive kidney. This fact demonstrates the possi- 

 bility of a neural contribution to the disturbed renal func- 



