RESISTANCE AND CAPACITANCE PHENOMENA IN VASCULAR BEDS 



947 



basis for autoregulation in skeletal muscle since it 

 was not abolished by breathing oxygen at either high 

 or low partial pressure. It should be noted that the 

 above conclusions regarding the myogenic theory are 

 based solely on negative evidence. It seems quite 

 unlikely to us that a vascular wall could respond 

 appropriately to changes of intraluminal pressure 

 per se. 



Physical factors related to autoregulation. Renal blood 

 flow at a given level of arterial pressure was the same 

 whether the perfusion pressure was steady or pulsatile. 

 Autoregulatory changes in resistance were observed 

 with both types of perfusion (93). 



A rise in renal interstitial and intrarenal venous 

 pressure was found to parallel an elevation of arterial 

 pressure over the ''autoregulatory range." This 

 finding is proposed as the explanation for the auto- 

 regulatory rise in renal vascular resistance that 

 accompanies an elevation of renal arterial pressure 

 (65, 96). On the other hand, two other groups of 

 investigators (81, 111) could not account for the 

 observed autoregulation in their dogs' kidneys on the 

 basis of such changes in intrarenal tissue or venous 

 pressures. 



An increase in postglomerular viscosity which 

 parallels glomerular filtration rate (116) has been 

 proposed to explain the ''autoregulatory" increase in 

 renal vascular resistance that accompanies a rise of 

 arterial perfusion pressure above 80 mm Hg. How- 

 ever, Selkurt et al. (100) found that arterial perfusion 

 pressure could be varied between 100 and 160 mm 

 Hg without significant change in blood flow (para- 

 minohippurate clearance), glomerular filtration rate 

 (creatinine clearance), or filtration fraction. In their 

 experiment, therefore, the postglomerular viscosity 

 remained unchanged, and the autoregulatory varia- 

 tion in renal vascular resistance must have occurred 

 solely in the preglomerular vessels. An increase in 

 effective viscosity of the blood flowing in the cortical 

 layers due to plasma skimming in the intralobular 

 arteries (cell separation theory) has been proposed by 

 Pappenheimer & Kinter (72, 87) to explain renal 

 autoregulation. However, Waugh & Shanks (111) 

 were able to demonstrate autoregulation in the kidney 

 using a cell-free perfusate, so long as the fluid con- 

 tained plasma. Evidently simple physical phenomena 

 will not serve to explain renal autoregulation. 



Enlargement of collateral communications following 

 occlusion of the cognate arterial supply as a manifestation of 

 autoregulation. It is well known that, following occlu- 

 sion of an artery, collateral communications between 

 the cognate bed and collateral arteries enlarge rapidly 



until within a few hours to weeks they can supply 

 almost a normal rate of flow to the cognate bed. Such 

 enlarged channels are demonstrated beautifully 

 during arteriography. The dilation of the communica- 

 ting channels may be considered a special case of 

 autoregulation, although almost nothing is known 

 regarding its mechanism of action. It does not appear 

 to be brought about by any special change in arterial 

 pressure proximal to the occlusion. The enlargement 

 of the communicating channels is more likely related 

 to an increased rate of flow or enhanced pressure drop 

 through the communicating channels (60). 



Summary of present status of feedback control of auto- 

 regulation. Though the mechanism of the autoregula- 

 tion of blood flow has not been established as yet, the 

 following trends may be stated, a) Most likely there 

 is more than a single factor involved and the pre- 

 dominant one may vary in different organs. In the 

 kidney, for example, maintenance of a constant 

 glomerular filtration rate may be more significant 

 than satisfaction of the metabolic requirements of the 

 organ; consequently the sensing mechanism to regu- 

 late blood flow should be related directly or indirectly 

 to glomerular filtration. The juxtaglomerular appa- 

 ratus may serve this function (97, 111). In organs 

 such as a skeletal muscle and the heart, metabolism 

 fluctuates rapidly; in these a mechanism must be 

 available to allow adaptation of flow to the varying 

 metabolic demands. Such mechanism should be 

 capable of sustaining the metabolic activity in the 

 face of fluctuations in arterial pressure. In either case 

 the sensing mechanism may detect the adequacy of 

 supply (i.e., tissue O a tension) or the adequacy of 

 removal of metabolic products (i.e., tissue CO2 

 tension). It appears probable that the former is sensed 

 in heart and muscle and the latter in the brain, b) 

 Autoregulation may be absent in vascular beds such 

 as the paw or skin which have very low metabolic 

 requirements, c) Whatever the mechanism of auto- 

 regulation, at times it appears to be dependent on the 

 presence of certain "normal factors" in plasma 

 required for maintenance of "normal vascular tone," 

 and at other times to be masked by certain "abnormal 

 factors" which may induce either "abnormally high" 

 or "abnormally low vascular tone." 



INTERPRETATION OF CHANGE OF VASOMOTOR TONE IN- 

 DUCED BY CONSTRICTOR AND DILATOR AGENTS IN VAS- 

 CULAR BEDS WHICH DEMONSTRATE AUTOREGULATION. 



In artificially perfused beds. When studying responses to 

 vasoconstrictor and vasodilator stimulation in a vas- 

 cular bed which demonstrates autoregulation it may 



