1500 



IIAMlBi )( iK OF I'HYSIOI OCA- 



CIRCULATION II 



Kobe/ 



Rinden- 

 Refleklomeler 



Y\^j Photozelle 



R 



Harnabfluss 



fig. 32. Method for measuring cortical and medullary cir- 

 culatory transit time. [After Kramer el al. (166).] 



table 12. Effect of Increased Perfusion Pressure on 

 Regional Transit Time of the Kidney 



Renal Art. 

 Pressure 

 mm Hg 



Med. Trans. 



Time (t p M) 



sec 



Cortical 



Trans. Time 



U.,R) sec 



t P M 

 1 P R 



Blood Flow 

 ml/g/min 



Urine Vol. 

 ml/min 



Experiment 



'°5 

 ■95 

 205 



16.5 



12. 1 



1 1 .2 



4.2 

 4-5 

 4-5 



0.25 

 2.50 

 3-5° 



Experiment 1 1 



[After Thurau et al. (308).] 



Ludwig's arterioles, could produce this effect.) The 

 total volume flow, they contend, is small relative to 

 total flow, and is within the error of the method of 

 measurement. Nevertheless, it suffices to "washout" 

 the osmotic gradient established in the critical long 

 vasa recta loops and accompanying loops of Henle in 

 the papillary zone. With this, the mechanism for 

 concentration of the urine becomes limited; and 

 diuresis ensues. Selkurt (276) has shown that this 

 type of diuresis is accompanied by enhanced sodium 

 excretion. 



In support of this hypothesis are the effects of water 

 diuresis and ADH action (fig. 33). Note the marked 

 decrease in medullary-plasma transit time (t p M) 

 with diuresis, and the return during ADH action. 



These effects are thought to be the result of changes in 

 blood viscosity brought about during water diuresis 

 (decreased concentration of albumin and cells in the 

 vasa recta) or increased ADH action. It will be re- 

 called that with water diuresis, lack of ADH activity 

 permits the urine to remain hypotonic: the osmotic 

 gradient is dissipated and, with it, no concentration 

 of blood constituents occurs: blood viscosity decreases, 

 and transit time is reduced. The vasopressor activity 

 of ADH (arginine-vasopressin) may conceivablv be 

 involved in regulation of blood flow in this circuit. 



The critical point of change in t,,M occurs when 

 Cosm — V — o, as revealed in two representative 

 experiments in figure 34. When free water clearance 

 (Ch 2 o) begins, T„M reaches a rather constant, minimal 

 value. 



The failure of Maxwell et al. (198) to note changes 

 in £p AH with diuresis and antidiuresis may have oc- 

 curred because the above changes in flow are small 

 enough not to be discernible in the normal range of 

 variation of the Ep XH measurement. 



An explanation of the results of Goodyer et al. ( 108, 

 log) may fall into line with the above findings. During 

 nonshocking hemorrhage during which arterial 

 pressure was kept constant, sodium excretion declined 

 in the absence of measurable changes in glomerular 

 filtration rate or renal plasma flow. (Data on urine 

 volume were not supplied, but this must certainly 

 have declined.) Measurement of intrarenal hematocrit 

 led them to conclude that intrarenal redistribution of 

 blood flow may have occurred, involving diversion of 

 plasma to cell-poor capillaries (or to lymphatic 

 spaces). This could involve the above mentioned vasa 

 recta mechanism, and obviouslv would be the con- 

 verse of the above cited experiments involving in- 

 creased renal perfusion pressure. 



In summary, a newly recognized and important 

 function of the vasa recta system as a counterpart of 



?r 



I' 



ml/min 

 80r 1 



few 



- *: 



" " 2 3 CStd. 



fig. 33. Mean medullary transit time of T-1824 (t p M) 

 during diuresis and after ADH; U/P„ sm : osmolar concentration 

 ratio of urine to plasma; GF: glomerular filtration. [After 

 Thurau et al. (309).] 



