I I'll 



HANDBOOK OF PHYSIOLOGY- 



CIRCULATION II 



decapsulation procedures, found that autoregula- 

 tion was indeed abolished (fig. 26). Haddy et al. (124) 

 illustrate several experiments which offer support of 

 this: two pressure-flow curves are more linear after 

 decapsulation than before. But Miles & DeWardener 

 (206) found no difference between the IRP of the 

 control and that of the decapsulated kidney. Elevation 

 of IRP by mannitol diuresis and elevation of venous 

 pressure caused approximately equal increases in 

 IRP in the decapsulated kidney and in the paired 

 control. In an extreme situation, following K.CN 

 treatment and elevation of perfusion pressure by 

 pump to 300 mm Hg, IRP increased ca. 100 mm Hg 

 in both control and decapsulated kidneys. 



In summary, the tissue pressure theory is attractive 

 in some respects, but since it concerns a purely phvsi- 

 cal mechanism it is hard to square with the lack of 

 autoregulation in kidneys treated with procaine, 

 KCN, and papaverine, in the oil-perfused kidney, or 

 even in dead kidneys. Implicitly, it dispenses with 

 the need for afferent arteriolar control, but a con- 

 siderable body of evidence supports the possibility of 

 such control. 



the myogenic theory. The principal evidence for 

 this theory comes from the behavior of the renal blood 

 flow during rapid changes in perfusion pressure. An 

 example taken from the work of Semple & 

 DeWardener (281) appears in figure 27. Flow was 

 measured with an electromagnetic flowmeter. Note 



I60> 



5CV 

 PV 



30SEC -v- 



fig. 26. Effect of decapsulation on autoregulation in the dog. 

 C: control; V: bilateral section of cervical vagosympathetic 

 chains in the neck; S: renal denervation; I): renal decapsula- 

 tion. [After Bounous et al. (28).] 



fig. 27. Renal circulatory adjustment following sudden in- 

 crease in arterial perfusion pressure i/ J .)i PI': renal venous 

 pressure. [After Semple & DeWardener (281).] 



the immediate "overshoot" of flow as pressure is 

 raised, followed by return to a flow level somewhat 

 below the control within 60 sec, and then stabilization 

 at the control flow but at a pressure some 50 mm Hg 

 higher than during the control. On occasion, rhythmic 

 rapid fluctuations in flow were observed after pressure 

 elevation before stabilization occurred, a "hunting" 

 phenomenon. 



When the elevation was done in progressive steps, 

 the overshoot was proportional to the pressure eleva- 

 tion, but returned in each instance to approximate 

 the control level [see fig. 28 (308)]. It is of interest 

 that the levels of flow, reached instantaneously after 

 pressure change, fall on a curve describing the 

 pressure-flow relationship in the same kidney after 

 paralysis of smooth muscle activity with papaverine 

 (x x in the figure). 



Likewise, when pressure was dropped in steps, flow 

 decreased immediately in a passive manner, but in 

 30 to 60 sec readjusted to the previous level [fig. 29 

 (120)]. In this series, constancy of flow was main- 

 tained down to 70 mm Hg, then fell off rapidly. 



Thurau & Kramer (307) have analyzed in an in- 

 teresting fashion the correlation of total blood flow, 

 superficial (cortical peritubular) capillary blood con- 

 tent, and weight change in response to rectangular 

 pressure increments. The results are illustrated in 

 figure 30. Capillary blood content was measured by 

 an "infrared reflectometer'" technique. Note the 

 typically instantaneous overshoot of flow as pressure 

 is increased, followed by stabilization. (Allowance 

 must be made for the possibility that an overshoot 

 artifact by the rotameter may contribute to the initial 

 rise.) This appears to be a function of the initial tonus 



