Effects of 24-Hour Unilateral Ureteral Obstruction on Glomerular Hemodynamics in Rat Kidney

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Kidney International, Vol. 15 (1979), pp. 457—462

Effects of 24-hour unilateral ureteral obstruction on glomerular hemodynamics in rat kidney

ANTONIO DAL CANTON, ARIBERTO CORRADI, RODOLFO STANZIALE, GIANFRANCO MARUCCIO, and LuIGI MIGONE

Seconda Clinica Medica, University of Parma, Parma, Italy

Effects of 24-hour unilateral ureteral obstruction on glomerular significativement. En conclusion l'obstruction uréterale deter- hemodynamics in rat kidney. Glomerular hemodynamics were mine, en 24 heures, une ischémie corticale importante qui n'est studied, by micropuncture, in Munich-Wistar rats submitted to pas rapidement reversible aprês Ia liberation de l'uretère. 24-hour unilateral ureteral ligation (UUL). Glomerular capillary pressure (PG), intratubular pressure (PT) and pressure in the first- order peritubular capillaries (EAP) were measured with a servo- nulling device. Single nephron filtration fraction (SNFF) was cal- Soon after ureteral obstruction, afferent arteri- culated from arterial and peritubular blood protein concentra- oles dilate, raising both plasma flow and hemo- tion. SNGFR was both measured by conventional micropuncture techniques and calculated from efferent arteriole blood dynamic pressure in glomerular capillaries, so that flow (EABF) and SNFF. Afferent arteriole blood flow (AABF) GFR is almost normally maintained in spite of a and resistance of afferent (Ra) and efferent (Re) arterioles were marked increase in intratubular pressure. Lessening calculated. Measurements were repeated I to 2 hours after the release of the ureter. Sham-operated rats were used as control. of the obstruction is followed rapidly by restoration UUL caused a marked increase in R (from 4.9[SD] 2.4 to of preobstructive conditions [1]. 12.7 5.1 dynes/sec/cm5). The fall in SNGFR (from 111.9 On the contrary, that afferent arterioles constrict [SD] 23.9 to 34.4 23.1 nl/minlkg body wt) was secondary to a decrease in both PG and AABF. A further increase in Ra (16.0 24 hours after ureteral ligation was suggested [2, 3]. 6.7 dynes.sec.cm5) occurred after releasing the ureter. SNGFR, No measurement, however, of GFR in the whole however, was unaltered (33.7 16.6 nI/mm/kg body wt) since kidney nor in the single nephron (SNGFR) has PG decreased parallel to PT, but AABF did not significantly change. Conclusion. Ureteral obstruction determines, in 24 been reported as yet in this condition. More ex- hours, a marked cortical ischemia that is not promptly reversed tensive studies were carried out after the release of by ureteral release. the ureter, showing a decrease in filtration rate as Effets d'une obstruction urétérale unilatérale sur l'hémo- well as in renal plasma and blood flow [4-10]. The dynamique glomérulaire dans le rein de rat. L'hémodyna- details of glomerular dynamics were not clarified, mique glomérulaire a été étudiée par microponctions, chez however, authors' efforts being mainly directed to- des rats Munich-Wistar soumis a 24 heures de ligature un- ilatérale de l'uretêre (UUL). La pression capillaire gloméru- ward elucidation of tubular function(s). laire (PG), la pression intratubulaire (PT), et la pression dans In this work our attention was focused on the gb- les capillaires péritubulaires de premier ordre (EAP) ont été merulus, with the purpose of contributing to a more mesurées au moyen d'un dispositif a zero asservi. La fraction de filtration des néphrons individuels (SNFF) a été calculée a partir comprehensive knowledge of renal function, both des concentrations de protéines dans le sang artériel et péritubu- during and after a sustained ureteral obstruction. laire. SNGFR a été mesuré a Ia fois par les techniques usuelles de microponction et calculC a partir du debit artériolaire efférent Methods (EABF) et de SNFF. Le debit artériolaire afférent (AABF) et les resistances des arterioles afférente (Ra) et efférente (R ont eté The experiments were carried out in a mutant calculés. Les mesures ont eté répétées une a deux heures après strain of Munich-Wistar rats having glomeruli on Ia liberation de l'uretère. Des rats ayant subi un simulacre d'operation ont été utilisés comme contrOles. UUL a déterminé the kidney surface [11]. Eighteen nonfasted rats, une augmentation importante de Ra (de 4,9 [sD] 2,4 a 12,7 5,1 dynes/sec/cm5). La diminution de SNGFR (de 119,9 [SD] 23,9 a 34,4 23,1 ni/mm/kg poids corporel) aété secondaire ala diminution a la fois de PG et de AABF. Une augmentation sup- Received for publication April 27, 1978 plémentaire de Ra (16,0 6,7 dynessec'cm5) est survenue apr- and in revised form October 4, 1978. ês Ia liberation de l'uretère. SNGFR, toutefois, n'a pas été af- fecté (33,7 16,6 nI/mm/kg poids corporel) du fait que PG a di- 0085-2538/79/0015-0457 $01.20 minué parallèlement a PT alors que AABF n'a pas change © 1979 by the International Society of Nephrology

457 458 Dal Canton et a! each weighing 160 to 290 g, were lightly anesthe- collected from the efferent arteriole and from a fern- tized with ether. The left ureter was ligated in 9 rats, oral artery. about 1 cm above the bladder, and the other 9 were Postobstructive studies. In 6 rats, when the mea- sham-operated and used for control. Twenty hours surements of the obstructive period were com- after these preliminary procedures, the rats were pleted, the left ureter was clamped just below the again anesthetized with sodium pentobarbital pelvis and was cannulated proximally to the ligation (Nembutal, 60 mg/kg body weight, i.p.) and were with a PE-50 tubing connected to a pressure trans- prepared for micropuncture as previously described ducer. The clamp was then released and ureteral [12]. After the surgical preparation, an i.v. infusion pressure (Pc) recorded. The obstruction was re- of bicarbonate-saline solution (sodium chloride, 110 lieved by cutting the PE-50 catheter used for P mEq/liter; sodium bicarbonate, 28 mEq/liter; potas- measurement. One hour was allowed before start- sium chloride, 5 mEq/liter) containing inulin (5%) ing the following measurements: (a) GFRs and so- was begun at an infusion rate of 0.02 mllmin, and dium excretion rates (UNUV) of both kidneys. Urine was maintained at that rate thereafter. One hour was collected under mineral oil from the left ureter was allowed for equilibration before micropuncture and from the bladder (for the right kidney) through measurements were started. PE-50 catheters. Arterial blood samples were ob- Ureteral obstruction studies. In 9 rats with 20- tained from the femoral artery at the beginning and hour unilateral ureteral ligation (UUL), glomerular at the end of clearance periods. (b) Micropuncture capillary pressure (PG),intratubularpressure (PT), measurements. Timed, complete collections of and pressure in first-order peritubular capillaries tubular fluid and of peritubular blood were carried (EAP) were measured with a servo nutting device out, and micropressures were recorded, as pre- (Instrumentation for Physiology and Medicine, San viously described. Diego, California) and were recorded simultaneous- Control studies. Measurements, as described ly with arterial blood pressure (BP) on a dual chan- above, were performed also on 9 sham-operated nel recorder (Hewlett-Packard, model 7702 B). rats, in whom the left ureter was handled in the Timed, complete collections of tubular fluid were same way as in the experimental group, except for performed together with arterial blood samples ligation. from a femoral artery for SNGFR measurement Analytical determinations. Urine volume was ob- [ii]. After the insertion of the pipette tip into the tained by weight. The volumes of fluid and blood tubule, an oil block (3 to 4 tubular diameters) was collected from proximal tubules and efferent arteri- injected, and collection was started by gentle as- oles, respectively, were estimated from the length piration and spontaneously continued thereafter. of the fluid column in a calibrated constant-bore Generally, collection was very slow, 5 to 15 mm quartz tubing of approximately 100 .tI.D.(Fried- being required to obtain adequate volumes of tubular rick and Dimmock, Millville, New Jersey, USA). fluid. Moreover, the oil block sometimes did not The concentration of chemical inulin in tubular fluid move downstream in the tubule, so that collection was measured by the microfluorescence method of of fluid was impossible. The number of collections Vurek and Pegram; chemical inulin concentrations (and of SNGFR measurements) being limited by in plasma and urine were determined by the di- these difficulties, SNGFR was calculated also from phenylamine method; plasma protein concentration the efferent arteriole plasma flow (EAPF) and single was measured by Lowry's method; a micro- nephron filtration fraction (SNFF) according to the adaptation of the same method was used to measure equation protein concentration in blood collected from efferent arterioles; sodium concentration in urine was SNGFR = -EAPF (1) measured by flame photometry [11]. 1—SNFF Calculations. SNGFR was calculated from Equa- tion I or measured according to This method, recently validated in our laboratory [1], does not require tubular collection, efferent ar- SNGFR =(TF/P)InV (2) teriole blood flow (EABF) (from which EAPF is cal- where (TF/P)InV refers to tubular fluid/plasma in- culated) being measured by timed complete collec- ulin concentration ratio and V to tubular flow rate. tion of blood from the efferent arteriole at its welling SNFF was calculated as point on the kidney surface, and SNFF being calculated from protein concentration in blood samples SNFF =1 3) Glomerular hemodynamics in ureteral obstruction 459 where Pa and Pc equal protein concentration in Re =(PG—EAP)/EABFx 7.962 x 1010 (12) blood samples collected from the femoral artery and (the factor 7.962 x IO° was used to express R in from efferent arterioles respectively. Efferent arte- units of dynes sec cm5, when pressures were riole blood flow (EABF) was obtained by timed expressed in mm Hg and flows in nl/min). Total ar- complete collection of blood according to teriolar resistance (RTA) was obtained by the sum totalcollected blood (nI) EABF = 4) RTARa+Re (13) collection time (mm) Transtubular pressure gradient (APT) was calcu- The microhematocrit in the efferent arteriole of su- lated as perficial nephrons (Hcte) was calculated according LPT =(PT+ Te) —EAP (14) to the expression Results Hcte = Ureteral obstruction studies. The results of these I l+(l—SNFF)x (5) studies are summarized in Table 1. PG fell from _i] 44.8(SD) 3.6 to 36.3 4.1 mm Hg (P <0.001). PT and Ta being unchanged, the decrease in PG was re- where HCta was the hematocrit measured in blood sponsible for the reduction in both LPG (from 31.4 samples collected from the femoral artery. Efferent 4.6 to 20.7 3.3 mm Hg, P < 0.001) and EFPa arteriole plasma flow (EAPF) was calculated ac- (from 17.25.6 to 7.8 3.4mm Hg, P < 0.001). A cording to the expression marked increase in Ra (from 4.92.4 to 12.7 5.1 EAPF =EABF(1 —Hcte) (6) dyne sec cm-5) determined a fall in both AABF (from 643.5 241.3 to 241.250.5 nllminlkg body Afferent arteriole blood flow (AABF), that is, the wt) and AAPF. Hence SNGFR was also markedly initial blood flow rate per glomerulus, was calcu- lowered, from 111.923.9 to 34.423.1 nI/mm/kg lated as body wt1 (P <0.001). AABF =EABF+ SNGFR (7) Ureteral obstruction caused a rise in Re and a decrease in both EAP and EABF. At the efferent end Afferent arteriole plasma flow (AAPF) or glomeru- of the glomerulus, gbomerular pressure equilibrium lar plasma flow (GPF) was derived from the ex- was taking place in control conditions and was pression maintained also during UUL, the ratio 1T€/LPGnot AAPF =GPF=AABF(1 —Hcta) (8) being different from 1 (P > 0.1). Pu rose from 5.1 2.2 to 15.44.1 mm Hg (P < The hydrostatic pressure gradient across the gb- 0.005), the latter value not being statistically dif- merular capillary (zPG) was defined as ferent from PT, during UUL. Finally, no difference — LPG =PG PT (9) was found in SNFF and 1PT, even though Pc and lTe were moderately lower during obstruction. Oncotic pressure at the afferent end (lTa)andat Postobstructive studies. The results of the post- the efferent end of the gbomerulus (?Te)wasde- obstructive studies are summarized in Tables 2 and rived from Pa and Pe, respectively, according to the 3. A further reduction of PG was caused by the re- equation of Landis and Pappenheimer [11]. Ef- lease of the ureter. PT, however, decreased parallel fective filtration pressure at the afferent end of the to PG, leaving unaltered both LPG and EFPa. Even glomerulus (EFPa) was calculated according to the though Ra increased from 10.6 2.2 to 16.0 6.7 expression dyne sec cm—5, a value bordering statistical sig- — EFPa ='G — PT lTa (10) nificance (0.01

Table 1.Pressures, flows, protein concentrations, hematocrits, and resistances in control conditions and after 24 hours of ureteral obstructiona

BP PG PT EAP PG AABF AAPF EABF EAPF SNGFR Body wt g mm Hg ni/rnin/kg bodywt Control 192.0 109.3 44.8 13.4 17.1 31.4 643.5 329.3 531.5 218.0 111.9 8.5

Ureteral 230.0 118.1 36.3 15.6 10.2 20.7 241.2 129.7 206.6 95.3 34.4 obstruction 10.2 50.5 28.9 I 49.8 26.0 P >0.05 >0.05<0.001>0.05<0.001<0.001 <0.001 <0.001 <0.001 < 0.01 <0.001 a Abbreviations used are: BP, arterial blood pressure; P, glomerular capillary pressure (hemodynamic); PT, intratubular pressure; EAP, pressure in the first-order peritubular capillaries; PG, hydrostatic pressure gradient across glomerular capillaries; SNGFR, single nephron glomerular filtration rate; AABF, afferent arteriole blood flow; AAPF, afferent arteriole plasma flow; EABF, efferent arteriole blood flow; EAPF, efferent arteriole plasma flow; Pa, systemic arterial protein concentration; Pe, efferent (peritubular capillary) protein concentration; Ta and Te oncotic pressure in afferent and efferent arteriole, respectively; EFPa, effective filtration pressure at the afferent end of the glomerulus; R and Re, resistance of single afferent and efferent arterioles, respectively; SNFF, single nephron filtration fraction; Hcta and HCte, hematocrit in afferent and efferent arteriole, respectively. All values are mean so. The results are given as mean values of the averaged measurements in single rats.

Table 2. Summary of pressures, flows, and resistances during ureteral obstruction and in postobstructive perioda P PT G EFPa SNGFR AAPF PT Ra Re mmHg ni/mm/kg body wt SNFF mm Hg dynes seccm Obstructive 35.2 13.6 21.5 8.3 41.5 142.5 0.29 21.8 26.1 10.6 4.1 period Postobstructive 28.2 9.5 18.7 7.8 33.7 122.2 0.28 17.8 20.6 16.0 4.7 period P <0.01 <0.01 >0.05 >0.1 >0.2 >0.1 >0.1 >0.05 >0.05 <0.05 >0.1 a Abbreviationsare definedin Table1. All values are mean so. The results aregiven as the mean values of the averagedmeasure- ments in single rats. Table 3. Urine flow, sodium excretion, and inulin clearance from prolonged ureteral obstruction and is maintained af- the right and the left (previously obstructed) kidney in ter the release of the ureter. This site of vasocon- postobstructive perioda striction was placed by some authors at the afferent Inulin clearance V UNaV arteriole, because of a decrease in stop-flow intra- mi/mm pi/min 1uEq/min tubular pressure [2, 3]. The results of our study Right kidney 0.910 3.82 0.72 clearly demonstrate that 20 hours after complete ureteral ligation an increase in afferent arteriole re- Leftkidney 0.155 2.94 0.59 sistance takes place, accounted for by a con- <0.05 >0.05 striction of the afferent arterioles. According to Poi- P <0.001 seuille's law, in fact, the resistance of a vessel is a Abbreviations used are: V, urine flow rate; UNaV, urine so- directly related to blood viscosity and to the length dium excretion. All values are mean so. of the vessel and is inversely related to the fourth 48.2 nllminlkg body wt in the postobstructive con- power of its radius. Although blood is a non-New- dition (Table 2). tonian fluid, its viscosity remains constant at physi- After releasing the ureter, GFR was markedly ologic flow rates for a given hematocrit and protein lower in the obstructed (left) kidney than it was in concentration [13]. Thus, since the latter values the contralateral one. This striking reduction in were unchanged during ureteral obstruction, and GFR (—83%) was accompanied only by a moderate assuming also that the length of the renal arterioles decrease in urinary volume (—23%), the slight de- was not modified, the increase in Ra is accounted crease in sodium excretion rate being not statistical- for by a reduction of the radius of the afferent arteri- ly significant (Table 3). ole, probably caused by a contraction of the muscle fibers of the wall. During ureteral obstruction, a rise Discussion was observed also in efferent arteriole resistance, Previous studies have given some evidence that although of minor extent. This cannot be fully ex- renal vasoconstriction takes place in response to plained by an increase in the muscular activity of Glomerular hemodynamics in ureteral obstruction 461

Table 1. (continued)

lTe EFPa Ra Re Hct HCte P Ta Pe APT g/100 ml mmHg gIIOOml mmHg iIAPG dynesseccm5 SNFF volume fraction mm Hg 4.56 13.7 7.50 29.4 17.2 0.95 4.98 2.73 0.37 0.485 0.604 24.5

4.37 13.1 6.01 20.7 7.8 1.02 12.70 4.68 0.26 0.460 0.539 25.9 7.1 >0.1 >0.1 <0.05 <0.05 <0.001 >0.1 <0.001 <0.025 >0.05 0.1 <0.025 >0.1 the wall, since anatomic studies, as well as physio- flow rate and sodium excretion was observed after logic data, have given evidence that the efferent ar- ureteral release. As the reduction in GFR overcame terioles of superficial nephrons behave as thin- that in SNGFR, a redistribution to superficial neph- walled venules [12, 14-17]. On the other hand, gb- rons, having short, salt-losing Henle's loops, may merular capillary pressure, that is, the hemo- have contributed to decrease fractional sodium and dynamic pressure of blood entering efferent arteri- water reabsorption. Proximal tubular reabsorption oles, was markedly reduced during ureteral ob- was not measured in our micropuncture experi- struction, whereas intratubular pressure, on which ments. The transtubular pressure gradient, how- interstitial pressure mainly depends, was un- ever, was not different from control conditions. changed; therefore, we can assume that the trans- Furthermore, others have given evidence that after mural pressure gradient was reduced and, accord- 24 hours of ureteral obstruction, proximal fractional ing to Laplace's law, that it contributed to decrease reabsorption, measured by micropuncture tech- the radius, that is, to raise the resistance of efferent nique, was increased rather than reduced [6]. We arterioles. may assume, therefore, that in our experiments the SNGFR was markedly lowered during ureteral fractional sodium and water reabsorption was de- obstruction. This is accounted for, in part, by the creased at more distal tubular sites. decrease in PG, and consequently, in effective filtra- Our study does not clarify the mechanism(s) re- tion pressure. Another main factor responsible for sponsible for vasoconstriction occurring after ure- the reduction in glomerular filtration was the fall in teral obstruction. Some persistent decrease in cor- glomerular plasma flow, the importance of the latter tical blood flow can be determined by surgical han- being increased by the occurrence of filtration pres- dling of the ureter [21]. These alterations, however, sure equilibrium [18, 19]. Since filtration pressure are admittedly of minor importance and cannot jus- equilibrium was maintained before and after relief tify the striking increase in arteriolar resistance tak- of obstruction, we cannot state whether any change ing place in rats with ureteral ligation, as compared in glomerular ultrafiltration coefficient plays a role to sham-operated controls. in the decreased GFR [20]. The increase in some peripheral vasoconstrictor The release of the ureter was followed by a fur- substance can be excluded as well, the control (the ther increase in afferent arteriole resistance, caus- right kidney) being not affected by contralateral ure- ing a reduction in glomerular capillary pressure. teral obstruction. On the other hand, a reduction in This, however, was compensated by a decrease in stop-flow intratubular pressure was demonstrated intratubular pressure, so that PG and EFPa rein single tubules blocked with mineral oil for 24 mained unchanged. The other major mediator of hours, suggesting that the response to tubular ob- change in nephron filtration rate, that is, glomerular struction occurs on an individual nephron basis [3]. plasma flow, was unmodified too, allowing SNGFR Single nephron hemodynamics seems to be regu- to be maintained at previous (obstructive) levels. lated by at least two hormonal systems having an- No further modification in Re was taking place in tagonist effects: the renin-angiotensin system and the postobstructive phase—according to the con- the renal prostaglandins. cept that efferent arterioles are almost devoid of According to the tubuloglomerular feedback hy- muscular activity—and because the transmural pres- pothesis, an increased sodium load to the macula sure gradient was unaltered, since both PT and PG densa results in local renin release and afferent arte- were decreasing in a parallel way. riole constriction; on the contrary, reduction of dis- A much greater decrease in GFR than in urine tal sodium delivery below normal values does not 462 DalCanton et a! measurably alter glomerular hemodynamics [221. uretic factors, including urea. 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