Capillary oncotic pressure as a modifier for tubuloglomerular feedback A. ERIK G. PERSSON, ROLAND MULLER-SUUR, (With the Technical Assistance of Birgitta Forsmark) Department

of Physiology

and Medical


PERSSON, A. ERIC G.,.ROLAND MILLER-SUUR, AND G~RAN SEL~N. Capillary oncotic pressure as a modifier for tubuloglomerular feedback. Am. J. Physiol. 236(Z): F97-F102, 1979 or Am. J. Physiol. 5(Z): F97-F102,1979. -Earlier experiments have shown that the sensitivity of the tubuloglomerular feedback mechanism can be reset. To study this resetting the effect of peritubular oncotic pressure on the sensitivity of the tubuloglomerular feedback mechanism was examined. Microperfusion experiments were carried out using Munich-Wistar rats. Proximal tubular stop-flow pressure (SFP) was measured in a nephron with a surface glomerulus, upstream to a solid paraffin block, while the downstream segment was perfused with Ringer solution (O-80 nl/min). Peritubular cap& illaries were perfused near the surface macula densa (100400 nllmin) with Ringer solution, ultrafiltrate of rat plasma, rat plasma, or remnant of rat plasma after’ ultrafiltration ([protein] about 10 g/100 ml). SFP at zero perfusion of the loop of Henle was unchanged compared to control at capillary microperfusion. ASFP,,, was the maximal reduction in SFP that could be released by the feedback mechanism. Ringer and ultrafiltrate perfusions decreased ASFP,,, to 2.3 & 0.6 (mean * SE) and 2.2 t 0.5 mmHg (control, 10.4 ? 0.9 and 9.4 t 1.1 mmHg), respectively. Remnant perfusion increased ASFP,,, to 14.3 t 3.1 mmHg (control, 7.0 2 2.3 mmHg), whereas plasma perfusion had no effect on ASFP,,, 8.4 t 1.5 mmHg (control, 8.0 t 1.3). It is concluded that the oncotic pressure in the peritubular capillary blood near the macula densa region determined feedback activity, probably by changes in interstitial pressure-volume conditions. tubuloglomerular feedback; stop-flow pressure; capillary microperfusion; colloid osmotic pressure; juxtaglomerular apparatus


nephron is that the distal tubule always returns to have close contact with its own glomerulus (21). This fact led Goormaghtigh (9) to suggest that some component of the distal tubular urine was sensed in the macula densa and that this information was then used to adjust the tonus of the nearby glomerular arterioles, giving a concomitant change in the glomerular blood flow and filtration rate. The possibility that such a feedback mechanism plays a role in the control of the glomerular filtration rate has been investigated intensively during the last decade. Rat experiments have yielded clear evidence of the existence of a mechanism that decreases proximal tubular stop-flow pressure, glomerular capillary pres0363-6127/79/0000-oooO$O1.25


0 1979 the American


AND GijRAN University


of Uppsala,


sure, and single nephron glomerular filtration rate if the flow to the distal nephron is artificially increased above normal (11,12,21,22,24). However, if the flow to the macula densa is reduced from normal to zero, most investigators do not find any change in the glomerular filtration rate under control conditions in the rat if salt intake exceeds certain limits (7). In the dog the reaction might be different (5). In the rat, therefore, the sensitivity of the feedback mechanism is very low at or below normal flow rates whereas at tubular flow rates just above normal the sensitivity is very high. The question has therefore arisen under what conditions the feedback is activated to reduce GFR. Davis and Freeman (6) in their review state that “evidence is lacking to demonstrate the physiological role for an intrarenal feedback mechanism in the control of single nephron GFR.” However, the studies of Dev et al. (7) and Kaufmann et al. (14) have shown that animals on a low sodium diet might have ‘a feedback-activated decrease in single nephron glomerular filtration rate, as indicated by a small difference in the measured nephron filtration rate between the proximal and distal tubule. Furthermore, Persson and Wright (19) have found that the reduction in total kidney GFR in acetazolamide diuresis is explained by feedback activation. In animals volume expanded with saline, Persson et al. (17) found that the feedback response elicited by load increase’ was diminished, thereby allowing the load to the distal nephron to increase above control values without activating the feedback. No resulting decrease in glomerular filtration rate therefore occurred. A similar mechanism might explain the absence of a difference in single nephron GFR measured in the proximal and distal tubule in plasma-volume-expanded animals (16). From these observations it appears as if the sensitivity of the feedback mechanism can be reset: In an attempt to elucidate how extracellular volume changes can be transmitted from the capillary side to cause a resetting of the juxtaglomerular apparatus (JGA) and modify the tubular signal, the following experiments were performed. The peritubular capillary network close to the macula densa was perfused with solutions with different colloid osmotic pressures. The effects of these perfusions were evaluated as the maximal drop in proximal tubular stop-flow pressure (SFP) at a suprathreshold tubular fluid load. The results showed that a high colloid concentration in the capillary perfusate increased the Society


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F98 feedback response, whereas a low colloid concentration decreased or abolished it. The change ofcapillary oncotic pressure could be mediated to the JGA by interstitial pressure changes, and the existence of an interstitial pressure volume receptor in the JGA is suggested. METHODS

Male and female rats of the Wistar WU strain (S. Ivanovas GmbH, Kissleg im Allgau, West Germany) weighing 150-200 g were used. This strain of rats, also called the Munich-Wistar strain, has accessible glomeruli on the surface of the kidney. Anesthesia was induced by intraperitoneal injection of Inactin (100 mglkg body wt). Arterial blood pressure was recorded via a catheter placed in the right common carotid artery. Three catheters were introduced into the right jugular vein for intravenous infusions. The left kidney was exposed through a flank incision, put into a Lucite holder, and fixed with a 3% agar solution. The kidney was superfused with preheated mineral oil to prevent drying of its surface. Throughout the experiment saline was infused intravenously at a rate of 4 ml/kg body wt per h. The micropuncture experiments were carried out as follows. A nephron with its glomerulus on the surface of the kidney was localized. The fmt nephron segment was identified, and with a technique described by Gutsche et al. (10) solid paraffin was injected into this segment to block the tubular fluid flow. Proximal to this block the tubular stop-flow pressure was recorded continuously, as a relative measure of glomerular capillary pressure, in Bowman’s space or in the fmt proximal tubular loop with a servo-nulling pressure recording device (8, 25). Distal to the block in the endproximal segment the nephron was perfused through a cannula containing end-proximal Ringer solution which was connected to a microperfusion pump. The microperfusion pump was connected to a Kulite microtransducer according to the method of Hierholtzer et al. (11). The composition of the end-proximal Ringer solution was 140 mM NaCl, 4 mM NaHC03, 4 mM KCl, 2 mM CaCl,, 1 mM MgClz, 7 mM urea, and 2 g/liter lissamine green. The stop-flow pressure was measured when the distal nephron was perfused from the end-proximal segment at perfusion rates which were varied from 0 to 80 nl/min. The maximal feedback response was calculated from the maximal drop in stop-flow pressure (ASFP,,) obtained when the flow to the distal nephron exceeded the threshold for feedback activation. Measurements were made both under control conditions and when the peritubular capillary network surrounding the macula densa was perfused with four different perfusion solutions. The capillary microperfusions were carried out as follows. A main branch peritubular capillary 3-8 tubular diameters from a visible macula densa on the surface of the kidney was selected. This capillary was punctured with a cannula containing one of the four perfusion solutions and connected via a small tube to a 50.~1 syringe driven by a Sage pump. The rate of capillary perfusion was adjusted so that both blood and perfusate were able to reach the macula densa area. This was done by allowing the border of a pale perfused area just to reach the macula densa. To achieve



this, different capillary perfusion rates were used, varying from 100 to 400 nl/min. In some instances the perfusate did not reach the macula densa but took other routes. These capillary microperfusions were used as controls to see what effect the microperfusion of capillaries belonging to other segments of the nephron than the macula densa had on the stop-flow pressure and on the maximal stop-flow pressure response. In no case were these parameters affected unless the capillary perfusion penetrated into the tubular system. In the event of a leak to the tubular system the nephron was not used further. It was therefore concluded with confidence that the observed effect only occurred when perfusions reached the macula densa area and did not represent an unspecific effect from perfusions of capillaries around other nephron segments. Puncture of the efferent arterioles of the nephron under investigation was avoided in order to prevent direct pressure ef%cts of the capillary perfusion on the glomerular capillary pressure. Before and after all capillary microperfusion periods control measurements without artificial capillary microperfwion were performed. In roughly half of the experiments another capillary perfusion with another solution was given at the same capillary site, with a postperfusion control measurement of the feedback response. The four capillary microperfusion solutions were I) Ringer solution, 2) ultrafiltrate of rat plasma, 3) rat plasma, and 4) remnant of rat plasma after ultrafiltration. The composition of the Ringer solution was 130 mM NaCl, 25 mM NaHC03, 4 mM KCl, 1 mM MgC1,, and 2 mM CaC12. Ultrafiltration of plasma was carried out with a roller pump at a pressure-difference of 1 atm across a Diaflo 20 M dialyzing membrane (Amicon, Lexington, MA). The gas mixture of 0, and CO, was adjusted so that a Pco2 of 40 mmHg was obtained. The ultrafiltration was performed immediately after centrifugation of blood drawn from the donor rats. The necessity for controlling Pco2 in the ultrafiltration process is due to the fact that changes in bicarbonate concentration will occur if Pco, falls, and such changes will affect the filtrability of other ionic constitr uents of plasma (E. Pallin and B. G. Danielson, unpublished observation). Before use the perfusion solutions were oxygenated by bubbling with a gas mixture of 95% O2 and 5% COB. The pH was adjusted to 7.4 by addition of HCl. The protein concentrations in the three perfusion solutions prepared corn rat p1asm.a were determined by the method of Lowry et al. (15). The protein concentration of the rat plasma was between 6.5 and 7.5 g/100 ml while in the ultrafiltrate of plasma it was less than 1 g/100 ml, and in the plasma remnant was about 10 g/100 ml. Arterial blood pressure was measured continuously throughout the experiment and was never allowed to fall below 100 mmHg. In cases when it did the experiments were discontinued. RESULTS

The original tracings from one experiment in which the capillary network surrounding the macula densa

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was perfused with two different solutions-remnant of plasma after ultrafiltration and ultrafiltrate of plasma-are shown in Fig. 1. Control measurements not shown in Fig. 1 were carried out between the two capillary perfusion periods. and after the second capillary perfusion. The figure shows the arterial blood pressure (BP), proximal tubular stop-flow pressure, the beginning and end of capillary perfusion, and the tubular perfusion rate (PR). It can be seen that the arterial blood pressure did not change during the experiment. With no tubular perfusion SFP remained unchanged, even though the peritubular perfusion was changed from 0 to 300 nl/min. In the control period when the end-proximal perfusion rate was increased over the threshold, there was a fall in SFP, with a maximum response of -6.5 mm.Hg. When capillary perfusion with plasma remnant was started and tubular perfusion was kept at zero, no change in SFP occurred. When the tubular perfusion rate was increased above the threshold for feedback activation there was a progressive increase in the maximal stop-flow pressure response with time (see Fig. 1). After a capillary perfusion time BP (mm Hg) 1SOr


SFP (mm Hg)


20 t



of 10 min a maximal response of -23 mmHg was reached. When the capillaries were perfused with ultrafiltrate of rat plasma, no change in SFP was detected at zero tubular perfusion rate, but the maximal feedback response diminished progressively almost to zero. From Fig. 1 it appears as if the effect of capillary perfusion increases with time. To test the time dependence of the capillary perfusion, the maximal stop-flow pressure response expressed in percentage of the initial control response was plotted against capillary perfusion time in Fig. 2. It was noted that the time dependence was variable, so that one nephron could reach a full response within 3-4 min while others needed more than 10 min. Nevertheless, all data were classified into three different groups: O-5 min, 5-10 min, and lo-15 min after the start of the capillary perfusion. Figure 2 shows the control values before and after perfusion and the response at three different times of perfusion. When a rat plasma ultrafiltrate was used, the maximal stop-flow pressure response was significantly lower (p < 0.001) in the period of lo-15 min than in the O- to 5-min period. Perfusions with plasma remnant gave a stronger response after l& 15 min than after O-5 min although the variability was high and the number of experiments small (P < 0.01). When plasma was used, no change in response was


- (a SFPmax 1ptrf (A SFPmax kontr

PR m fnl/min) *or


BP (mm Hgl









PR Wmin) 80



BP (mm Hg) 150



t SFP (mm Hgl

PR Wmin) *Of

0-5min I

1 mtn

FIG. 1. Original recordings from 1 tubule perfused with 2 solutions-ultrafiltrate of rat plasma and remnant of rat plasma af%er ultrafiltration. Figure shows arterial blood pressure (BP), proximal tubular stop-flow pressure (SFP), tubular perfusion rate (PR), and beginning and end of capillary microperfusions.



po”I Pm conir.

FIG. 2. The ratio (ASFP,,),~/(ASFP-),,,l, is the ratio of maximal stop-flow pressure at capillary microperfusion ((ASFP,,)& to that under control conditions ((ASFP,&,,&. Values are given from different time periods after start of capillary perfusion and are related to preperfusion control values. Postperfusion control values are also given. Capillary perfbsates: A, plasma; 0, remnant of plasma; o, ultrafiltrate of plasma; l , Ringer solution.

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FlOO noted. In all experiments the control values after perfusion did not differ significantly from the initial control. Table 1 and Fig. 3 summarize the results from all experiments. Table 1 gives blood pressure, the stopflow pressure at zero tubular perfusion with and without capillary microperfusion, and also the maximal feedback response (ASFP,,,), i.e., the stop-flow pressure decrease at suprathreshold tubular perfusion rates. The ASFP,,, for each individual nephron was averaged from 3 to 10 stimulations for the control situation without microperfusions of the capillaries. The ASFP,,, values during capillary microperfusion were obtained at the end of the capillary perfusion period when the effect was at its maximum. It is evident from Table 1 that the mean ,stop-flow pressure values did not differ from each other during the different periods. Therefore, the capillary perfusion itself did not induce any change in stop-flow pressure. ASFP,,, (Table 1 and Fig. 3) decreased significantly (P < 0.01) when Ringer solution was perfused, and in 3 of 12 tubules with ultrafiltrate of plasma no stop-flow pressure response at all was detected when tubular flow was increased to 80 nl/min. Thus the feedback activity completely disappeared. After the experimental period ASFP,,, returned to control level. When plasma was used to perfuse the capillaries no change in ASFP,,, was found between the control period, the capillary perfusion period, and the postperfusion control period. Capillary perfusion with plasma remnant induced a significant increase (P c 0.001) in ASFP,,,. The control values after plasma remnant perfusion approached the preperfusion control level. Arterial blood pressure was not significantly different between the groups. DISCUSSION

The validity of proximal tubular as a relative measure of glomerular

stop-flow capillary

pressure pressure

TABLE 1. Effect on SFP and maximal feedback response with different capillary perfusates compared with control values before and after perfusions Capillary



Ringer solution (n = 18)

4Z?d =& --


Control SFP, -g



Control SFP, -Hg

Af!zg, 9.1

125 23.2

37.0 21.7

10.4 kO.9

35.1 k2.1

2.3* +0.6

36.2 22.2


Ultrafiltrate of rat plasma (n = 12)

120 22.6

36.8 k1.7

9.4 Al.3

37.5 21.3

2.2* 20.5

35.8 21.7


Remnant of rat plasma

111 t6.6

36.3 t1.6

7.0 i12.3

35.8 21.6

14.3* 23.1


5.1 to.7

128 26.1

37.4 8.0 22.0 1 21.3







(n = 6)

Rat plasma

k1.9 21.5 21.4 t2.0 Values are means f; SE. SFP, stop-flow pressure; ASFP,,, maximal feedback response. *P < 0.01 compared with the control situation. (72 = 4)



















FIG. 3. Mean maximal stop-flow pressure response (ASFP, mmHg) at capillary microperfusion with 4 different solutions compared with mean control values before and after microperfusion.

seems to be well established from earlier investigations. Theoretically the glomerular capillary .pressure minus the colloid osmotic pressure of plasma should equal the proximal tubular stopflow pressure if reabsorption of fluid from the proximal tubule is negligible and if the increase in tubular pressure does not induce a vascular reaction with changes in the arteriolar tone. In our series of experiments the proximal tubular solid paraffin block was placed very close to the glomerulus, usually in the first loop, and the stop-flow pressure was measured either in Bowman’s space or in the first loop just above the block. Reabsorption of fluid, therefore, had been negligible. It has also been found that under control conditions the directly measured glomerular capillary pressure values in Munich-Wistar rats (2, 7) and in Sprague-Dawley rats (13) agree well with the values of tubular stop-flow pressure plus the colloid osmotic pressure of plasma. Accordingly, proximal tubular stop-flow pressure appears to be an adequate relative measure -of glomerular capillary pressure and represents a technique for determining the effect of tubuloglomerular feedback activity. The capillary microperfusions were carried out with all four -perfusion solutions in the following way. A capillary some tubular diameters from the macula densa was selected, and the perfusion rate was adjusted so that the macula densa visible on the surface of the kidney was perfused both with perfwate and with blood. The capillary perfusion rate, therefore, varied from 100 to 400 nl/min from tubule to tubule. Adjustment of the capillary perfusion rate in this way seemed essential for at least two reasons. First, Agerup (1) has

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shown from experiments with capillary microperfusions that at a perfusion rate of 250 nl/min a capillary pressure increase of 3-5 mmHg in the vicinity of the perfusion pipette occurred. Obviously, this pressure head must decrease in the periphery of the perfused area to approach the normal capillary pressure at the border against the blood-perfused areas, since superficial capillaries form a continuous network of communications. To ensure a normal or nearly normal hydrostatic pressure, it is essential to locate the macula densa in the border of the perfused area. Second, blood is also mandatory for proper oxygenation of the macula densa. Oxygen bubbling of the perfusate will increase oxygen tension, although the oxygen content may still be insufficient. Since blood also perfused the macula densa, and since the perfusate was oxygenated and, moreover, the oxygen dfision rate was relatively rapid, it seems unlikely that the macula densa would have suffered from lack of oxygen during the perfusions. -With such capillary perfusions -with -both-blood and perfusate-reaching the macula densa it is impossible to determine exactly the protein concentration of the fluid passing the macula densa, although this concentration is well known in the perfusate. The results must therefore be regarded as a qualitative estimate of how changes in colloid concentration can effect the tubuloglomerular feedback control of the glomerular filtration rate. The present results show that a decline of oncotic pressure in the capillary fluid outside the juxtaglomerular apparatus, induced by perfusion of Ringer solution or ultrafiltrate of rat plasma, significantly decreased the maximal feedback response, and in about a third of the experiments totally blocked the feedback activity. On the other hand, a rise in colloid osmotic pressure with use of remnant of rat plasma after ultrafiltration significantly increased the maximal feedback response. When plasma was used as a capillary perfusate, no change in this response was detected. It should be noted that the capillary perfusion itself did not affect the tubular stop-flow pressure. Only the maximal response to a suprathreshold load of fluid to the distal nephron induced by increased perfusion through Henle’s loop showed a change. The mechanisms by which the change in colloid concentration can affect the feedback response is unclear. One possible explanation could be that the effect is mediated from the capillary side to the macula densa via pressure-volume changes in the interstitial space. However, other explanations such as a direct effect on the JGA cells by some constituent in the protein fraction cannot be excluded. An interesting observation was that the effect of the perfusion was increased progressively during the 5- to 15min perfusion period. The time dependence of capillary perfusion on the resetting of the function of the juxtaglomerular apparatus might indicate either a slowly responsive capillary receptor for colloid osmotic pressure or a second fluid compartment mediating the effect. Morphological studies have given no clear evidence for a direct capillary receptor and, therefore, the second explanation seems more plausible. A possible intermediary fluid compartment could be the



local interstitial spaces located between the capillaries and the tubular and glomerular cells. Changes in pressure or volume in these interstitial spaces could take some time to develop and might explain the timedependent effect. A decrease in capillary oncotic pressure would then, due to impaired capillary uptake of fluid, be able to induce an increase in interstitial fluid volume, with a higher hydrostatic and lower oncotic pressure (26, 27). A rise in capillary oncotic pressure, owing to an increased fluid uptake in the capillaries, would induce a reduction in interstitial pressure. The mechanism underlying the way by which the changes in interstitial pressure and volume can affect the function of the juxtaglomerular apparatus is still a matter for speculation. Widening of the interstitial spaces may render the information transfer from the macula densa cells to the rest of the juxtaglomerular apparatus difficult (3), or a change in the interstitial pressure conditions might alter the cell volume, with a resulting change in cellular transport processes. These pressure and volume changes could either influence the effector cells in the juxtaglomerular apparatus or the receptor cells in the macula densa. In either case, from the present experiments a receptor function of the juxtaglomerular apparatus can be suggested. It was observed by Persson et al. (18) that volume expansion with saline (5% saline/kg body wt) reduced the maximal feedback response, and therefore GFR did not decrease by feedback action. Such a resetting could also explain the absence of a feedback response observed when no proximal-to-distal difference in single nephron GFR in plasma volume-expanded animals was found (16), although the distal load considerably exceeded the normal. The present experiments add further knowledge to the question of a resetting of the tubuloglomerular feedback mechanism. Indeed, it may be suggested that changes in extracellular fluid volume might regulate the feedback activity via alterations of the interstitial pressure and volume conditions. Therefore, in a situation with dehydration or hypovolemia of another origin an increased capillary uptake would reduce the interstitial volume and also diminish the hydrostatic pressure, whereas the oncotic pressure would tend to increase. These changes would then, in turn, activate the tubuloglomerular feedback, which could reduce GFR. In saline volume expansion a decreased capillary fluid uptake would increase the local interstitial fluid volume and the interstitial hydrostatic pressure, and decrease the interstitial oncotic pressure. These changes would then affect the juxtaglomerular apparatus, with. a decreased feedback activity as a result. To investigate this question further, our laboratory (18) measured both the maximal feedback response and the threshold for end-proximal flow rate at which the feedback mechanism is activated in dehydrated, control, and volume-expanded animals. It was found in that study that the maximal stop-flow pressure response was increased during dehydration and decreased during volume expansion. The threshold for activation of feedback was decreased during dehydration and increased during volume expansion, quite in accordance with the result in the present study.

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F102 We would like to propose that the theory for the macula densa function is extended by an interstitial pressure-volume receptor mechanism. When the load on the distal nephron is sensed at the macula densa site the response from the JGA apparatus is dependent on the stimulation of the interstitial receptor. It could be suggested that in a situation with volume depletion, for example, feedback activation is agumented (18) and consequently the feedback mechanism can be activated and can reduce GFR even though the distal load might be normal or subnormal. Accordingly, the feedback control is activated as a consequence of the extracellular fluid needs and not only as a result of an increase in distal fluid delivery. Furthermore, if the observation of Steinhausen et al: (23) of a countercurrent system for




cortical blood flow, i.e., a flow of peritubular capillary blood from the distal end of the proximal tubule towards the proximal end, is correct, a decreased fluid absorption in the proximal tubule and the loop of Henle would increase colloid osmotic pressure in the blood perfusing the macula densa and, hence, activate the feedback mechanism. This mechanism would then act with the tubuloglomerular feedback to potentiate the response of the glomerular filtration rate. Address reprint requests to Dr. Eric Persson, Dept. of Physiology and Medical Biophysics, Biomedicum, Box 572, S-751 23 Uppsala, Sweden. Received 6 June 1977; accepted in final form 20 September 1978.

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352: 315-337,1974. 12. ISRAELIT, A.,

F. RECTOR, AND D. SELDIN. The influence of perfusate composition and perfusion rate on glomerular capillary hydrostatic pressure (Abstract). Proc. Ann. Meet. Am. Sot. Nephrol., 6th., Washington, DC, 1973, p. 53. 13. KALLSKOG, o., L.-O. LINDBL~M, H. R. ULFENDAHL, AND M. WOLGAST. .Kinetics of the glomerular ultrafiltration in the rat kidney. An experimental study. Acta Physiol. Stand. 95: 293300,1975. 14. KAUFMANN,


I. S., K. J. HAMBURGER, AND W. FLAMENBAUM. Tubuloglomerular feedback: effect of dietary NaCl intake. Am. J. Physiol. 231:*1744-1749, 1976. LOWRY. 0. H.. N. J. ROSEBROUGH. A. L. FARR. AND R. J.

RANDALL. Protein measurement with the Folin phenol reagent. J. Biol. Chem. 193: 265-275,195l. 16. MADDOX, D. A., J. L. TROY, AND B. M. BRENNER. Autoregulation of filtration rate in the absence of macula densa-glomerulus feedback. Am.‘J; Physiol. 227: 123-131,1974. 17. PERB~ON, A. E. G., J. S~HNERMANN, AND F. S. WRIGHT. Eff’ed of isotonic volume expansion on feedback control of glomerular filtration rate. Proc. Int. Congr. Physiol. Sci. 26th, New Delhi, 1974, p. 119. 18. PERSBON, A. E. G., G. SELBN, AND R. MUELLER-SUUR. Activation of the tubulo-glomerular feedback in dehydrated animals. Proc. Int. Congr. Physiol. Sci., 27th, Paris, 1977, p. 589. 19. PERSSON, A. E. G., AND F. S. WRIGHT. Reduction of glomerular filtration rate by intrarenal feedback during acetazolamide diuresis (Abstract). Federation Proc. 33: 805, 1974. 20. PETER, K. Die Nierenkanalchen des Menschen und einiger SPugetiere. Anut. Anz. 30: 114-124,1907. 21. S~HNERMANN, J., A. E. G. ~?ERs~~N, AND B. AGERUP. Tubuleglomerular feedback. Non-linear relation between glomerular hydrostatic pressure and loop of Henle perfusion rate. J. Clin. Xnvest. 52: 862-869, 1973. 22. SCHNERMANN, J., F. S. WRIGHT, F. S. DAVIS, J. M. STACKELBERG, AND G. GR.ILL. Regulation of superficial nephron filtration rate by tubulo-glomerular feedback. Pfluegers Arch. 318: 147175,197o. 23. STEINHAUSEN, M., G. M. EISENBACK, AND R. GALASKE. A counter-current system of the surface of the renal cortex of rats. Pfluegers Arch. 318: 244-259,197O. 24. THURAU, K., AND J. SCHNERMANN. Die Natriumkonzentration an den Macula densa-Zellen als regulierender Faktor f%.r das Glomerul~ltrat (Mikropunktionsversuche). KZin. Wochenschr. 43: 410-413,X%5. 25. WIEDERHJELM, C. A., J. W. WOODBURY, S. KIRK, AND R. RUSHMER. Pulsatile pressures in the microcirculation of frog mesentery. Am. J. Physiol. 207: 173-176,1964. 26. WOLGAST, M., E. PERSSON, J. SCHNERMANN, H. ULFENDAHL, AND P. WUNDERLICH. Colloid osmotic pressure of the subcapsular interstitial fluid of rat kidneys during hydropenia and volume expansion. Pfluegers Arch. 340: 123-131,1973. 27. WUNDERLICH, P., E. PERBSON, J. SCXNERMANN, H. ULFENDAHL, AND M. WOLGAST. Hydrostatic pressure in the subcapsular interstitial space of rat and dog kidneys. Pfluegers Arch. 328: 307-319.1971.

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Capillary oncotic pressure as a modifier for tubuloglomerular feedback.

Capillary oncotic pressure as a modifier for tubuloglomerular feedback A. ERIK G. PERSSON, ROLAND MULLER-SUUR, (With the Technical Assistance of Birgi...
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