Distribution Of Cortical Blood Flow Research Articles

Visualization of the intrarenal distribution of capillary blood flow.

This study describes a modified technique to fill the renal vasculature with a silicon rubber (Microfil) compound and obtain morphologic information about the intrarenal distribution of capillary blood flow under a variety of conditions. Kidneys and cremaster muscles of rats were perfused in vivo with Microfil using a perfusion pressure equal to the animal's mean arterial pressure at body temperature. Microfil did not alter arteriolar diameter or the pattern of flow in the microcirculation of the cremaster muscle. The modified protocol reproducibly filled the renal vasculature, including; glomerular, peritubular, and vasa recta capillaries. We compared the filling of the renal circulation in control rats with that seen in animals subjected to maneuvers reported to alter the intrarenal distribution of blood flow. Infusion of angiotensin II, hypotension, volume expansion, and mannitol‐ or furosemide‐induced diuresis redistributed flow between renal cortical and medullary capillaries. The advantage of the current technique is that it provides anatomical information regarding the number, diameter, and branching patterns of capillaries in the postglomerular circulation critical in determining the intrarenal distribution of cortical and medullary blood flow.

A1651 TAURINE IMPROVES REDUCED RENAL MEDULLARY BLOOD FLOW IN SPONTANEOUSLY HYPERTENSIVE RATS

Objectives: Present study was carried out to clarify the effect of renal nerve stimulation on renal cortical and medullary blood flow and the effects of chronic treatment of taurine on altered renal cortical and medullary blood flow distribution by renal nerve stimulation in spontaneously hypertensive rats (SHR). Methods: We used 6–7 (young) and 16–17 week old (adult) SHR and divided to taurine treated group and control group. Renal nerve surround left renal artery was stimulated electrically by 2, 5, 10 and 15 Hz under the anesthesia of isoflurane. Renal blood flow was measured using laser tissue flow meter using noncontact prove for cortical blood flow and contact glass-fiber needle type of prove for medullary flow. After a series of electrical stimulation, 1 mg of LNAME was injected and same protocol was repeated. Results: High frequency stimulation caused transient cortical blood flow elevation and which was followed by decrease of blood flow in young and adult WKY. In contrast, blood flow in renal medulla showed no significant changes compared with that in cortex. Young SHR showed a decrease of cortical and medullary blood flow by nerve stimulation. In adult SHP, blood flow reduction was similar to young SHR and medullary blood flow was more reduced than that in young rats. In adult WKY and young SHR, LNAME augmented the reduction of medullary blood flow by electrical stimulation. In adult SHR, LNAME showed no effects on blood flow reduction in medulla. Chronic treatment of taurine blunted the reduction of blood flow by electrical stimulation in medulla but not in cortex of adult SHR. Conclusion: Medullary blood flow is protected through the nitric oxide production in normotensive rats but this mechanism is blunted in SHR. Taurine could improve the reduction of renal medullary blood flow in aged SHR.

Congential obstructive nephropathy gets complicated

Most young children with end-stage renal failure are born with abnormal kidneys1,2, predominantly with renal dysplasia, a term describing a histopathologic spectrum featuring a block in normal differentiation (e.g., poor collecting duct branching and failure to generate glomeruli and nephron tubules) and aberrant differentiation (e.g., lineage switching to form smooth muscle and cartilage)2,3. The term "congenital obstructive nephropathy" describes kidney malformations associated with obstructed urinary tracts4. In many cases, lesions affect only one of the two renal tracts, and, in these cases, end-stage renal failure does not develop. Such lesions include atretic ureters associated with multicystic dysplastic kidneys and ureterocoeles associated with dysplasia of upper components of duplex kidneys. In other cases, when urinary flow impairment occurs later in gestation, or when obstruction is partial (e.g., pelvic-ureteric junction obstruction), renal damage is less profound, although fibrosis and atrophy can occur. On the other hand, when fetal urine flow is impaired bilaterally, the clinical implications are severe, with end-stage renal failure a possibility. In such cases the obstructing lesion is generally distal to the urinary bladder (e.g., posterior urethral valves), a lesion almost unique to males4. The latest epidemiologic data from the United Kingdom indicate that approximately 750 children are being treated for end-stage renal failure. Renal dysplasia without obstruction accounts for 22% of these individuals, while congenital obstructive nephropathy with posterior urethral valves accounts for another 14% (Personal communication, M. Lewis, Report of the Pediatric Renal Registry, 2002).

In Vivo Fluorescence Microscopy of Microcirculation in the Renal Cortex of Mice

In vivo fluorescence microscopy was used in experimental studies of renal cortical microcirculation in mice. The effects of i.v. infusions of mannitol and iohexol were studied in normal and obese/hyperglycemic mice and in mice with streptozotocin-induced diabetes mellitus. All infusions produced marked effects on the distribution and velocity of cortical blood flow with no differences between iohexol and mannitol. The renal cortical blood flow was inhomogeneous regarding different capillaries and there was an initial rise in the number of capillaries with increased blood flow after infusions of both mannitol and iohexol. The infusions of contrast medium were initially followed by a significantly larger number of capillaries with decreased blood flow in the obese/hyperglycemic mice (p < 0.05) than in the diabetic and nondiabetic mice. The variations in obese/hyperglycemic groups were, however, large. The effects were the same in normal and diabetic animals.

Assessment of the distribution of renal cortical blood flow by contrast ultrasonography

The importance of the distribution of intrarenal blood flow in the regulation of various renal functions, such as urine concentration and sodium excretion, has been well recognized. However, there have been no reliable methods to measure local flow in the kidney in vivo. The present study demonstrated the usefulness of contrast ultrasonography combined with injection of sonicated 5% albumin for assessment of the distribution of renal cortical blood flow in eleven mongrel dogs. The left kidney was displayed by tomographic echography, and microbubbles of sonicated albumin were injected into the abdominal aorta above the left renal artery. Video density time curves were generated and fitted to a time-intensity curve. Intrarenal infusion of acetylcholine (4.0 micrograms/kg/min) increased renal blood flow (RBF) from 2.5 +/- 0.3 to 4.6 +/- 1.0 ml/min/g kwt (p < 0.01), and norepinephrine (0.5 microgram/kg/min) decreased RBF from 2.5 +/- 0.3 to 1.2 +/- 0.5 ml/min/g kwt (p < 0.01). There were significant positive correlations between percent change in RBF and peak intensity and area under the curve, which were calculated with a time-intensity curve. Furthermore, the inner/outer renal cortex ratio of peak intensity significantly increased during acetylcholine infusion (0.72 +/- 0.11 vs 0.86 +/- 0.09; p < 0.01), whereas no significant change was observed during norepinephrine infusion. These results suggest that renal contrast ultrasonography may be useful for real-time assessment of the distribution of renal cortical blood flow in vivo.

In vivo fluorescence microscopy of microcirculation in the renal cortex of mice

In vivo fluorescence microscopy was used in experimental studies of renal cortical microcirculation in mice. The effects of i.v. infusions of mannitol and iohexol were studied in normal and obese/hyperglycemic mice and in mice with streptozotocin-induced diabetes mellitus. All infusions produced marked effects on the distribution and velocity of cortical blood flow with no differences between iohexol and mannitol. The renal cortical blood flow was inhomogeneous regarding different capillaries and there was an initial rise in the number of capillaries with increased blood flow after infusions of both mannitol and iohexol. The infusions of contrast medium were initially followed by a significantly larger number of capillaries with decreased blood flow in the obese/hyperglycemic mice (p < 0.05) than in the diabetic and nondiabetic mice. The variations in obese/hyperglycemic groups were, however, large. The effects were the same in normal and diabetic animals.

In Vivo Fluorescence Microscopy of Microcirculation in the Renal Cortex of Mice

In vivo fluorescence microscopy was used for experimental studies of the renal cortical microcirculation in mice. The effects of i.v. infusions of mannitol and iohexol were studied in untreated mice as well as in mice after temporary renal ischemia. All infusions produced marked effects on the distribution and velocity of cortical blood flow with no differences between iohexol and mannitol. The renal cortical blood flow was inhomogeneous with respect to different capillaries and there was an initial rise in the number of capillaries with increased blood flow after infusions of both mannitol and iohexol. There was an initial increase in the number of capillaries with a decreased blood flow following 30 min of ischemia. This increase was reduced by both types of infusions, suggesting a beneficial effect on renal cortical blood flow. Neither mannitol nor contrast medium exhibited any adverse effects in ischemic kidneys that would be likely to affect renal function. However, 5 min after the infusions there was an increasing number of capillaries with decreased blood flow in all groups.

In Vivo Fluorescence Microscopy of Microcirculation in the Renal Cortex of Mice

In vivo fluorescence microscopy was used for experimental studies of the renal cortical microcirculation in normal mice and in mice pretreated with the nephrotoxic drug cyclosporin A. The cortical circulation was studied after i.v. infusions of a nonionic low osmolar contrast medium (iohexol) and after infusions of mannitol. All infusions produced marked effects on the distribution and velocity of cortical blood flow with no differences between iohexol and mannitol. The renal cortical blood flow was inhomogeneous regarding different capillaries and there was an initial rise in the number of capillaries with increased blood flow after infusions of both mannitol and iohexol. There was simultaneously an increased number of capillaries with decreased blood flow following all infusions. The decreased blood flow after infusion of iohexol was more pronounced when the animals had been pretreated with cyclosporin A. The difference was only significant (p < 0.05) during a short part of the observation period of 30 min, but it may indicate that kidneys previously exposed to cyclosporin A are more susceptible to infusions of iohexol.

In Vivo Fluorescence Microscopy of Microcirculation in the Renal Cortex of Mice

In vivo fluorescence microscopy was used for experimental studies of the renal cortical microcirculation in mice. The effects of i.v. infusions of mannitol and iohexol were studied in untreated mice as well as in mice after temporary renal ischemia. All infusions produced marked effects on the distribution and velocity of cortical blood flow with no differences between iohexol and mannitol. The renal cortical blood flow was inhomogeneous with respect to different capillaries and there was an initial rise in the number of capillaries with increased blood flow after infusions of both mannitol and iohexol. There was an initial increase in the number of capillaries with a decreased blood flow following 30 min of ischemia. This increase was reduced by both types of infusions, suggesting a beneficial effect on renal cortical blood flow. Neither mannitol nor contrast medium exhibited any adverse effects in ischemic kidneys that would be likely to affect renal function. However, 5 min after the infusions there was an increasing number of capillaries with decreased blood flow in all groups.

EFFECTS OF CHRONIC CYCLOSPORINE ADMINSTRATION ON RENAL BLOOD FLOW AND INTRARENAL BLOOD FLOW DISTRIBUTION

Cyclosporine-induced decreases in renal blood flow (RBF) and glomerular function are well documented. Glomerular filtration and tubular function may be affected by changes in both total renal blood flow and cortical blood flow distribution (CBFD). The effect of CsA on RBF, CBFD, glomerular filtration rate, and tubular function was studied in conscious ewes receiving a mean CsA dose of 30 mg/kg/day for 28 days with mean CsA trough levels of 344 +/- 45 ng/ml. RBF and CBFD were determined by the injection of 15 microns radioactive microspheres before and after one month of treatment with CsA or its vehicle, olive oil. RBF decreased by 24% from 7.65 +/- 0.87 to 5.79 +/- 0.42 ml/min/g of kidney in CsA-treated ewes (P = 0.014), while no decrease was noted in the control group (7.92 +/- 1.10 vs. 7.62 +/- 0.71). Intracortical blood flow decreased in proportion to the fall in total renal blood flow--thus CsA treatment did not change the cortical distribution of flow. There was a 25% decrease in GFR, as determined by inulin clearance, in the CsA-treated group (80 +/- 6 vs. 62 +/- 3 ml/min; P = 0.027) while there was a nonsignificant increase in control animals (62 +/- 11 vs. 92 +/- 7 ml/min). There was no evidence of tubular dysfunction in either group. There were also no changes in urinary excretion rates of prostaglandins PGE2, 6-keto-PGF1 alpha or thromboxane B2, nor were there changes in plasma renin activity. CsA induced decreases in RBF occur red without redistribution of cortical blood flow, indicating that altered cortical distribution of blood flow is not responsible for the changes in GFR or tubular function that have been reported. The changes in renal blood flow and glomerular filtration rate are independent of changes in renal prostaglandin production, and are likely not associated with altered plasma renin activity.

Cortical blood-flow in the porcine kidney. A radioactive microsphere study.

Renal cortical blood-flow distribution was measured by means of radiolabeled microscopheres in eight kidneys from 4 pigs of mixed Yorkshire and Danisk landrace. We found a pronounced intracortical variation in the perfusion pattern of 28 sections of outer cortex. Three consequetive flow determinations with an interval of 45 minutes showed that the heterologous perfusion pattern was plastic, changing between the flow-determinations. In addition, we found a significantly reduced perfusion in the renal poles, compared to the rest of the outer cortex. It is speculated that the reduced polar perfusion is a contributing aetiological factor to the increased incidence of polar scar formation secondary to reflux nephropathy.

Role of prostagalandins in the cortical distribution of renal blood flow following reductions in renal perfusion pressure

The purpose of this study was to examine the role of prostaglandins in the redistribution of renal cortical blood flow that occurs following reductions in renal perfusion pressure. The distribution of blood flow to the renal cortex was examined using radio-labeled microspheres (15 ± 1 μm). It was found that in animals not treated with a prostaglandin synthesis inhibition a decrease in renal perfusion pressure to the limit of renal blood flow autoregulation was associated with a decrease in fractional flow to the outer cortex (Zone I) and an increase in fractional flow to the inner cortex (Zones III and IV). A further decrease in renal perfusion pressure below the limit of autoregulation produced a further decrease in the fractional flow to Zone I and a further increase in fractional flow to Zones III and IV. In contrast, in animals treated with the prostaglandin synthesis inhibitor meclofenamate (5 mg/kg, i.v. bolus) a reduction in renal perfusion pressure to the limit of renal blood flow autoregulation produced no change in fractional blood flow to any of the 4 cortical zones. A further decrease in renal perfusion pressure, however, did produce a fall in fractional blood flow to Zone I and an increase in fractional flow to Zones III and IV. In conclusion, the results of this study indicate that within, but not below, the limit of renal blood flow autoregulation prostaglandin synthesis is an important factor in the regulation of renal cortical blood flow distribution.

Renal cortical perfusion--preliminary experience with the dynamic spatial reconstructor (DSR).

The three-dimensional image data generated by the Dynamic Spatial Reconstructor (DSR) enables measurement of the three-dimensional distribution of blood supply in organs. We have applied this imaging technique to evaluate renal cortical blood flow distribution and compare it with distribution of radiolabeled microspheres. The DSR, a high temporal resolution volumetric roentgenographic computed tomographic scanner, was used to scan the volume containing a kidney in 0.13-0.26 s and repeating this scan 8-4 times per s for six s during a renal arteriogram. Five anesthetized dogs were studied in the prone position with the left kidney exteriorized through a flank incision. An electromagnetic flowmeter was placed around the renal artery and a needle placed retrograde into the artery for injection of a 2 cc bolus of contrast agent. During the scan the contrast agent was injected over a four s period during which radioactively labelled microspheres were injected into the left atrium. The tomographic images of approximately 10 parallel, 5 mm thick sagittal slices corresponding to the slices of the kidney used for counting microspheres in the cortical layers were displayed and analyzed. The time point chosen for analysis was the one in which peak brightness (i.e., concentration of contrast agent) was detected in the cortex. The spatial distribution of peak brightness values was compared to the number of microspheres at the same sampling locations. The microsphere-based value of regional cortical blood flow fell below the regression line for the juxtamedullary cortex and above for the outer cortex. This result is consistent with the preferential distribution of microspheres to the outer cortex whereas the contrast agent distributed more uniformly throughout the cortex.

Inner medullary hemodynamics in chronic salt-depleted dogs.

The effects of chronic salt depletion on medullary hemodynamics remain unknown. In the present study, sodium excretion, renal hemodynamics including papillary plasma flow, measured by the albumin-accumulation technique, and papillary tissue solute content were determined during hydropenia in 13 anesthetized sodium-replete and 10 sodium-depleted dogs. Salt depletion induced a significant rise in plasma renin activity and aldosterone without potassium depletion. Mean arterial pressure, GFR, and renal blood flow were similar in sodium-depleted and sodium-replete dogs. Despite a similar distribution of cortical blood flow (measured by the microsphere method) in the two groups, papillary plasma flow was markedly reduced in sodium-depleted dogs (8.8 +/- 1.7 vs. 22.8 +/- 1.9 ml X min-1 X 100 g-1 in sodium-replete dogs), associated with a significant decrease in renal sodium excretion. Furthermore, papillary osmolality and sodium concentration were significantly greater in sodium-depleted dogs. Ultrastructure examination revealed smooth muscle cells surrounding the efferent arterioles and pericytes with contractile potential encircling descending vasa recta. These results suggest that included in the complex hemodynamic adjustment to chronic sodium depletion is a significant reduction in inner medullary blood flow that may be important in maintaining enhanced papillary solute concentration. In addition, the anatomy of the medullary vasculature is compatible with regional regulation of medullary blood flow.

Hemodynamic adaptation to reduced renal mass in early postnatal development.

Radioactive microspheres, clearance methodology, and glomerular counting techniques were used to compare hemodynamic changes resulting from uninephrectomy at birth with those of sham-operated guinea pigs 8-13 days of age and 18-24 days old. Left renal blood flow doubled from 10-20 days of age, and was approximately 65% higher in animals with reduced renal mass. Cardiac output also doubled from 10-20 days of age but was not significantly affected by uninephrectomy whereas mean arterial blood pressure rose with normal or compensatory renal growth. There was a progressive fall in renal vascular resistance that paralleled the drop in total peripheral resistance during normal growth, but the fraction of cardiac output supplying the remaining kidney of renoprival guinea pigs rose significantly from 7% at 10 days to 11% at 20 days of age. Whole kidney filtration fraction averaged 0.25-0.29 for all groups. There was no change in cortical blood flow distribution with age or after uninephrectomy: 50, 30, and 20% supplied outer, middle, and inner thirds, respectively. Glomerular perfusion rate increased proportionately in all cortical levels during normal or compensatory renal growth, and was higher in outer and inner cortical thirds than in the middle cortex. It is concluded that systemic and intrarenal hemodynamic responses to uninephrectomy at birth are similar to the pattern of normal maturation. Reduction in renal mass and normal somatic growth provide additive stimuli resulting in maintenance of homeostasis.

Intrarenal Vascular Effects of Angiotensin II and Angiotensin III in the Dog

The effects of intrarenal bolus injections of equal molar doses of angiotensin II and angiotensin III on renal blood flow were examined in seven pentobarbital anaesthetized dogs. Renal blood flow was measured with an electromagnetic flow probe. Angiotensin II produced a greater decrease in renal blood flow than angiotensin III at all bolus doses tested when the integral of the renal blood flow response was examined. In 10 other dogs, we compared the molar dose of intrarenal constant infusions of angiotensin II and angiotensin III required to decrease total renal blood flow by approximately 25%. The effect these peptides had on the distribution of renal cortical blood flow was determined with radioactive microspheres. In the constant infusion experiments, more moles of angiotensin III than angiotensin II were required to produce a given decrease in renal blood flow in each experiment. The average percent decrease in blood flow to each of the four cortical zones produced by angiotensin II was not different from that produced by angiotensin III. Our data demonstrate that angiotensin II is more potent than angiotensin III as a vasoconstrictor in the renal vasculature.

Skimming of microspheres in vitro: implications for measurement of intrarenal blood flow.

Skimming could result in erroneous estimation of renal cortical blood flow distribution as measured by microspheres. Skimming of microspheres with diameters 10, 12, and 15 micrometers and red blood cells was therefore studied in a model in which an interlobular artery and its first arteriolar branch were simulated by 80- and 30-micrometers-wide slits between glass prisms. The experiments were performed with citrated blood at a hematocrit (Hct) of 40, flow velocities of 3 and 6 cm/s, and branch flow varying from 2 to 25%. At a branch flow fraction comparable to that of a deep arteriole in the dog kidney (3%), Hct in branch blood was 24% lower than that of input blood, whereas 10-, 12-, and 15-micrometers microsphere concentrations were 75, 81, and 87% lower, respectively. The size-dependent skimming was probably caused by wall exclusion in the main channel. Differences in particle inertia did not affect skimming. The results suggest that the disparate local flow values obtained by use of microspheres of different sizes in dog and rat kidneys are due to a size-dependent skimming of the microspheres.

Intrarenal vascular effects of angiotensin I and angiotensin II.

The effects of angiotensin I (250 pmol) and angiotensin II (7.5 pmol) on total renal blood flow and its cortical distribution were examined in 25 dogs anesthetized with pentobarbital. These peptides were administered as bolus injections directly into the left renal artery. Right and left renal blood flows were measured with noncannulating electromagnetic flow probes. The distribution of renal cortical blood flow was measured with 15-micrometers radioactive microspheres. Because angiotensin I is converted to angiotensin II extrarenally as well as intrarenally, the distribution of renal blood flow in response to the bolus injection of angiotensin agonists was measured before these peptides could have recirculated through the kidney. This maneuver precluded the possibility that blood flow changes were due to the extrarenal formation of vasoactive metabolites of angiotensin I or angiotensin II. Control total renal blood flow averaged 3.0 +/- 0.1 ml.min-1.g kidney wt-1 and was decreased 25% by both angiotensin I and angiotensin II. Outer renal cortical flow (zone I) was 5.1 +/- 0.3 ml.min-1.g-1 and was decreased to 3.9 +/- 0.3 ml.min-1.g-1 by both angiotensin I and angiotensin II. On the average, angiotensin I decreased inner cortical renal blood flow from a control of 1.8 +/- 0.2 to 1.2 +/- 0.2 ml.min-1.g-1; angiotensin II decreased inner cortical renal blood flow from a control of 1.9 +/- 0.2 to 1.4 +/- 0.2 ml.min-1.g-1. Analysis on a per-experiment basis revealed that angiotensin I, compared with angiotensin II, produced a proportionally greater decrease in inner cortical renal blood flow relative to its effects on outer cortical blood flow.

Effect of arachidonic acid and indomethacin on renal function of dogs with pericardial tamponade.

Previous studies revealed persistent sodium retention in dogs with chronic pericardial tamponade (induced by injection of Freund adjuvant into pericardial sacs) and pericardiocentesis, revealed in increased sodium excretion. Three groups of dogs were studied. Group 1 was treated with indomethacin (2.5 mg/kg, iv) prior to pericardiocentesis. Compared with experiments without indomethacin, sodium excretion did not increase flowing pericardiocentesis in animals treated with indomethacin despite similar changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity. This effect of indomethacin was presumably mediated through prostaglandin (PG) synthesis inhibition. Group 2 dogs received an infusion of arachidonic acid (AA) (to increase PG synthesis) into the left renal artery (20 micrograms.kg-1. min-1). Sodium excretion increased after AA infusion during tamponade (11.2 to 30.9 mequiv.min-1) with a further increase occurring after pericardiocentesis (84.4 mequiv.min-1). Animals in group 3 were infused with both 20 and 80 micrograms. kg-1. min-1 doses of AA. Although sodium excretion following 80 micrograms.kg-1.min-1 AA(21 mequiv.min-1) was higher than that seen during 20 micrograms.kg-1.min-1 (14.2 mequiv.min-1), a further increase in sodium excretion to 45.6 mequiv.min-1 followed pericardiocentesis. During tamponade, AA did not change any of the measured parameters other than sodium excretion, a result compatible with the proposed distal tubular site of action of PG. Absolute but not fractional cortical blood flow distribution increased during the time sodium excretion increased following pericardiocentesis in all experiments. It is proposed that increased PG synthesis may be one possible mechanism involved in the natriuresis seen following pericardiocentesis. One cannot exclude the possibility that increased absolute blood flow to the superficial cortex also contributes to the observed natriuresis. Changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity appear to contribute to the observed natriuresis but only when PG synthesis is not blocked.

ISCHEMIC ACUTE RENAL FAILURE: ENHANCED RECOVERY OF SUPERFICIAL NEPHRON FUNCTION BY ATP-MGCL2

The infusion of ATP-MgCl2 will enhance the recovery from an ischemic renal insult. To define the role of intratubular obstruction and hemodynamic factors in the recovery process, rats were subjected to 45 minutes of bilateral renal artery occlusion and infused with either ATP-MqCl2 (25 μmoles) or 0.9% saline (NS). In ATP-MgC12 treated animals, whole kidney GFR (WKGFR) was significantly greater (550 ± 46 μl/min/100 gmBW) than NS infused animals (286 ± 32, P < 0.01) although both values were less than controls (1107.8 ± 51.4). Superficial single nephron GFR (SNGFR) attained control values (45.6 ± 2.2 μl/min) in ATP-MgCl2 treated animals whereas SNGFR was 50% of control values in NS treated rats (22.6 ± 2.1, P < 0.01). The return of SNGFR to normal values while WKGFR remained reduced was not related to intratubular obstruction since proximal tubular pressure was not significantly different in either group (11.8 ± 0.3 in NS and 10.8 ± 0.3 in ATP-MgCl2, P = NS). The relative changes in SNGFR and WKGFR could be related to hemodynamic factors. Although total renal blood flow was similar in both groups (5585 ± 282 μl/min/100 gmBW), the proportion of flow to the outer cortex was significantly increased in ATP-MgCl2 treated animals (1.94 ± 0.06, P < 0.01) as compared to NS (1.51 ± 0.03). Thus, the enhancement of recovery of GFR in superficial nephrons appears to be related to cortical blood flow distribution rather than intratubular obstruction.