THE RENAL CIRCULATION 



'497 



and humoral factors, gave support to the myogenic 

 theory, and he concluded "Vascular tone is in its 

 basic origin myogenic, though strongly influenced by 

 external factors." 



That this property of the smooth muscle of the kid- 

 ney arterioles is typical of smooth muscle elsewhere 

 is shown by the work of Bozler (30). Isolated segments 

 of ureter were subjected to sudden increases in in- 

 ternal pressure. This created electrical potentials 

 which produced, at first, local responses; if the poten- 

 tial was strong enough, a conducted response resulted. 

 He found that the greater the pressure, the steeper 

 was the local potential change and the shorter the 

 delay for the onset of conduction. Bulbring (43) has 

 shown that stretch of smooth muscle cells of the taenia 

 coli acted as a stimulus for increased myogenic auto- 

 maticity, and that the element of the smooth muscle 

 cell sensitive to stretch was closely combined with the 

 properties of the tension-producing element. 



The group of investigators that support the 

 myogenic theory to explain autoregulation of the 

 kidney favor the afferent arteriole as the site of regula- 

 tion. More specifically, the myocytes of the juxta- 

 glomerular apparatus appear to be a likely point of 

 control (274, 331). In conclusion, the myogenic 

 theory seems most attractive as an explanation of 

 autoregulation of the renal circulation, but it is likely 

 that acceptance of one theory to the exclusion of some 

 of the others would be an oversimplification. The 

 challenging prospect remains to integrate properly 

 the several possibilities into a unified concept which 

 might operate in the intact, unanesthetized animal in 

 normal circulatorv homeostasis 



PRESENT STATUS OF THE TRUETA 

 JUXTAMEDULLARY SHUNT 



It was postulated by Trueta et al. (311) that diver- 

 sion of renal blood from its usual cortical route to the 

 "less resistant and more capacious medullary circuit" 

 (198) (probably not true by currently known facts) 

 was a physiologic mechanism which was involved in a 

 number of abnormal circulatory states. These in- 

 cluded reflex anuria, anuria associated with incom- 

 patible blood transfusion, crush injury, blackwater 

 fever, etc., Pitressin inhibition of water diuresis, the 

 renal ischemia of shock or that induced by fright or 

 adrenaline, in the reduction in tubular excretion 

 following protracted renal ischemia, and in the genesis 

 of essential hypertension. 



These investigators had reported that during renal 



ischemia the arterial pulse may be seen in the renal 

 vein, and that the renal venous blood may acquire an 

 arterial color. It was their belief that the juxtamedul- 

 lary glomeruli and vasa recta circuit may afford 

 veritable shunts between the renal artery and vein "... 

 a diversion of blood from the cortex, the most active 

 part of the kidney, to the medullars- pathway, with a 

 possible increased speed of flow through these 

 channels." 



Such shunts should therefore cause a reduction in 

 renal oxygen A-V difference. Furthermore, this would 

 shunt blood away from the zone ol greater metabolic 

 activity in the cortex to the juxtamedullary vasa recta 

 and loop of Henle system, with less efficient perfusion 

 of the proximal tubular secretory sites. This should 

 cause a decrease of E D or £ PAH with an increase, or 

 no necessary decrease, in total blood flow as measured 

 by direct methods or perhaps by the Fick method. 

 Finally, if shunts open which bypass glomeruli, £ In 

 should decrease without a decrease in blood flow, or 

 should decrease more markedly than blood flow 

 (assuming continued adequacy of filtration pressure). 



Morphological identification of the shunt should be 

 possible with injections of India ink, Prussian blue, or 

 radiopaque material such as Thorotrast. The Trueta 

 evidence consisted mainly of appearance of India ink 

 or Thorotrast in higher concentration in the juxta- 

 medullary region when injected intravascularly during 

 sciatic nerve stimulation or epinephrine action. But 

 great care must be exercised in attempts to interpret 

 rate or volume of flow by appearance of the injection 

 mass. Thus, contraction of venous effluent constrictors 

 could give the appearance of congestion of the medul- 

 lary circuit, in the face of an actual reduction of flow. 

 Incomplete filling due to faulty injection could give 

 the appearance of vasoconstriction in the cortex. 



Morphological Evidence 



Injection studies have been controversial, being 

 interpreted either in favor of the original hypothesis or 

 against it. This has been largely a matter of interpreta- 

 tion of what are often quite similar pictures. 



Montague & Wilson (214), correlating Thorotrast 

 injection studies with clearance data (£ PAH ) in rabbits, 

 believed they saw evidence of a juxtamedullary shunt 

 after epinephrine injection. This was accompanied 

 by marked decreases in E Fxn (mostly negative, and 

 averaging — 26.6^). Herdman & Jaco (138) par- 

 tially constricted one renal artery of rabbits, and in- 

 jected India ink 3 days to 5 weeks later. They found 

 the ink chiefly in the inner cortex and juxtamedullary 



