THE RENAL CIRCULATION 



•477 



fig. 23. Estimates of hydrostatic pressures (mm Hg) in 

 the dog nephron and associated vasculature [After Swann 

 (342, discussion).] 



(P V( ) pressures are measured, and the A-V difference 

 calculated. 



In 15 experiments on the kidney (nerves intact) 

 (352), P Af averaged 12.0 ± 4.1 (sd) mm Hg, and 

 Pv t , 5.0 ± 2.9. The P Af — P v , difference was 7.0 

 ± 3.6 mm Hg. Another series (4) agreed very closely. 

 The minimum arterial pressure for flow (Pa,), in 

 this situation corresponding to critical closing pres- 

 sure, was of the same order of magnitude as the 

 "yield pressure" in the dog (7-14 mm Hg) (120, 

 258, 271, 282). 



Arterial pressure flow (P A( ) (preferred to CCP 

 because of the probability of inherently different 

 connotation) and P A( — P V| can be experimentally 

 varied under a variety of circumstances. The values 



table 3. Relation Between Intratubular and Peritubular 

 Capillary Pressure in Unmanipulated Kidneys 



* Adjusted for rat differences by the statistical technique 

 of disproportionate subclass numbers in the analysis of 

 variance. [After Gottschalk & Mylle (112).] 



are lowered by nerve section and ganglionic block- 

 ing agents. They are increased during the reflex 

 response to carotid occlusion and noradrenaline 

 intra-arterial injections and to cooling (352). 



The role of tissue pressure is of importance, particu- 

 larly as influenced by the renal venous pressure and 

 the possibility of a venous-arteriolar reflex. It was 

 found that when pressure-time curves were deter- 

 mined at venous pressures of 15 to 60 mm Hg (4), 

 that P A( and P Vf became identical in 8 of 12 cases, 

 and in the remaining 4 ranged from 2 to 6 mm higher 

 than venous pressure (P v ) at the end of 2 to 2.5 min 

 of occlusion. 



The P Af at elevated venous pressure was never 

 greater than the sum of the control P Af and the applied 

 venous pressure, implying a lack of increase in vaso- 

 motor tone as the result of increasing venous pressure, 

 and arguing against a venous-arteriolar reflex. 



Identical pressure at the elevated venous pressure 

 implies that the distensible resistance vessels have 

 increased their caliber or in some manner permitted 

 the pressure to equilibrate. In the four cases with con- 

 sistently higher P A( an explanation of "prevailing 

 high vasomotor tone alone or in combination with an 

 initially high intrarenal pressure" was offered. In 

 any event, Astrom believes that the interstitial pres- 

 sure in the kidney is more important than the vaso- 

 motor tone as a determinant of the P Af and the 

 P A( — P Vf difference. 



Hinshaw et al. (141) related the apparent CCP to 

 tissue pressure changes in dog kidneys. Stabilized 

 values following clamp of inflow and after cessation 

 of flow were 1 . 7 mm Hg, for P A — P v pressure dif- 

 ference, and 2.9 mm Hg for tissue pressure. The 

 correspondence of values led them to the conclusion 

 that the A-V pressure differences were the result of 

 the tissue pressure; the somewhat higher value for the 

 tissue pressure indicated incomplete transmission of 

 pressure across the walls of the vessels. At any rate, the 

 manifest CCP could be accounted for by the tissue 

 pressure, they believed. If so, then the active vaso- 

 motor tone would be negligible in the kidney under 

 these experimental conditions. This conclusion held 

 for kidneys in situ (nerves intact) as well as their 

 pump-lung-kidney preparations. 



The conclusion reached by Astrom was that CCP 

 in the kidney in the sense employed by Burton need 

 not be assumed and that the P A( more appropriately 

 should be considered as a yield pressure, that pressure 

 needed to start flow against the compressing effect 

 of the interstitial pressure. It should be added here 

 that the term "yield pressure" as originally employed 



