Quantitative assessment of proximal tubule function in single nephrons of the rat kidney

Bm, Brenner; Tm, Daugharty; Ueki, IF; Troy, JL

doi:10.1152/ajplegacy.1971.220.6.2058

Cited by 41 publications

(14 citation statements)

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“…Recent studies from this laboratory have yielded evidence to indicate that the natriuresis which accompanies acute Ringer's loading in the rat is attended by marked expansion of plasma volume and corresponding dilution of pre-and postglomerular plasma protein concentration (2,3,5). In contrast, the results of the present study demonstrate that the natriuresis of chronic Ringer's loading is associated with only mild expansion of plasma volume and little reduction in pre-and postglomerular plasma protein concentration.…”

Section: Discussioncontrasting

confidence: 76%

“…There is abundant evidence in the rat to indicate that the natriuresis that attends the acute expansion of extracellular volume with colloid-free solutions is associated with an increase in the rate of delivery of proximal tubule fluid to more distal segments of the nephron, an effect due both to a rise in glomerular filtration rate (GFR)1 and a fall in absolute proximal reabsorption (1)(2)(3)(4)(5). The latter change has been shown to be causally mediated, at least in part, by the accompanying dilutional reduction in postglomerular vascular protein concentration (3).…”

Section: Introductionmentioning

confidence: 99%

“…From these measurements, single nephron GFR (SNGFR) and the absolute rate of tubule fluid reabsorption to the site of puncture were calculated, using equations previously described (6). Quantitative collections of tubule fluid were obtained using the technique of controlled suction previously validated for this laboratory (2 (6,7), and from these measurements, single nephron cortical filtration fractions (SNFF) were calculated (6). At the completion of each study both kidneys were weighed.…”

Section: Introductionmentioning

confidence: 99%

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Renal Response to Chronic Intravenous Salt Loading in the Rat

Daugharty¹,

Ueki²,

Nicholas³

et al. 1973

J. Clin. Invest.

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A B S T R A C T The natriuresis of acute Ringer's loading is associated with a rise in the rate of delivery of fluid beyond the proximal tubule due both to a rise in glomerular filtration and a fall in absolute reabsorption, the latter being causally mediated, at least in part, by the accompanying fall in postglomerular vascular [protein]. To determine whether these factors also contribute to the renal response to chronic Ringer's loading, nine rats given continuous infusions, 30% body weight/ day over 5-14 days, were studied using free-flow micropuncture techniques. Results were compared with data from 10 chronic control rats given less than 1.5% body wt/day. Late proximal tubule fluid-to-plasma [inulin] ratios, (TF/P) IN, single nephron glomerular filtration rate (SNGFR), absolute proximal reabsorption, and postglomerular vascular [protein] in chronic control rats and chronically loaded rats averaged 2.2± SE 0.1 (n=35) and 1.5±0 (35), P<0.001; 37+-2 (35) and 47±4 nl/min (35), P < 0.05; 19±1 (35) and 16±2 nl/min (35), P > 0.2; and 9.5±0.3 (8) and 8.6±0.3 g/100 ml (8), P > 0.05, respectively. Thus the fall in (TF/P)IN and the rise in distal delivery during chronic Ringer's loading were due almost entirely to the rise in SNGFR, and not to any large fall in absolute reabsorption. Hence chronic and acute Ringer's loading increase delivery of proximal tubule fluid by different mechanisms, with chronic sodium homeostasis being governed overwhelmingly by adjustments in GFR.

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Section: Discussioncontrasting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Renal Response to Chronic Intravenous Salt Loading in the Rat

Daugharty¹,

Ueki²,

Nicholas³

et al. 1973

J. Clin. Invest.

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“…These first and last segments, examined to determine whether inulin leaks out of proximal tubules as a result of isehiemic injury, were identified by observing the passage of lissamine green which was injected rapidly (0.04 ml of a 5% solution) into the left jugular vein. Tubule fluid was collected with sharpened micropipettes (8-12 jsm OD), using the technique of controlled suction previously validated for this laboratory (7). In addition, two to three samples of femoral arterial blood were obtained for determination of hematocrit and plasma inulin concentration.…”

Section: Methodsmentioning

confidence: 99%

“…-PC RE = EABF X (7.962 X 1010) (7) Total arteriolar resistance for a single pre-to postglomerular vascular unit: RTA = RA + RE (8) Estimates of the net ultrafiltration pressure (Pup) at the afferent-and efferent-most portions of the glomerular capillary:…”

Section: Methodsmentioning

confidence: 99%

Dynamics of Glomerular Ultrafiltration in the Rat V. RESPONSE TO ISCHEMIC INJURY

Daugharty¹,

Ueki²,

Mercer³

et al. 1974

J. Clin. Invest.

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A B S T R A C T An experimental model of postischemic, acute renal failure has been developed in Wistar rats with surface glomeruli, thereby making possible a direct assessment of the mechanisms responsible for the fall in glomerular filtration rate that characterizes this disorder. Whole kidney and cortical single nephron filtration rates were reduced proportionately, on average by approximately 40%, after 3 h of nearly complete occlusion of the ipsilateral renal artery. The possibility of a significant transtubular leak of inulin was excluded. This decline in filtration rate occurred in the absence of measured changes in mean arterial pressure, mean glomerular transcapillary hydrostatic pressure, or net ultrafiltration pressure at afferent and efferent ends of the glomerular capillary. Net ultrafiltration pressure at the efferent end of the capillary approached zero both before and after ischemic injury, demonstrating that filtration pressure equilibrium was achieved throughout this study. Single nephron filtration fraction remained unchanged, indicating that the fall in filtration rate was accompanied by a proportional decline in glomerular plasma flow. The results indicate that the fall in filtration rate was solely the consequence of this fall in glomerular plasma flow. Since filtration rate per nephron is equal to the product of the ultrafiltration coefficient and mean ultrafiltration pressure, this product must also have fallen in proportion to the decline in glomerular plasma flow. Evidence is presented to indicate that a change in ultrafiltration coefficient is not required to This work has been published in abstract form. 1973. Clin. Res.

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Renal Micropuncture Techniques

Velázquez

Wright

1992

Comprehensive Physiology

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The sections in this article are: Animal Subjects Equipment, Tools Dissecting Microscopes Compound Microscopes Pipette Pullers and Grinders Capillary Glass, Micropipettes Syringes, Tubing Micromanipulators Microperfusion Pumps Infusion Pumps Heated Micropuncture Tables Pressure Transducers Specialized Surgical Equipment Scintillation Counters Voltmeters Electrodes Recorders Oil and Wax Blocks Wax Injection Apparatus Timers In Vivo Micropuncture: Functional Assessment of Individual Nephron Segments Anesthesia and Surgery Evaluation of Kidney before Micropuncture Micropipette Placement Identification of Accessible Cortical Tubules and Vessels Identification of Papillary Structures Measurement of Distance to Puncture Site and Length of Perfused Tubule Determination of Filtration and Transport Rates Determination of Blood Constituents Measurement of Capillary and Tubule Pressure Potential Problems Micropuncture in Nonstandard Preparations Microanalytical Techniques Volume Inulin Protein Urea Osmolality Metal Cations Halide Anions Ammonia Carbon Dioxide and Bicarbonate

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Quantitative assessment of proximal tubule function in single nephrons of the rat kidney

Cited by 41 publications

References 0 publications

Renal Response to Chronic Intravenous Salt Loading in the Rat

Renal Response to Chronic Intravenous Salt Loading in the Rat

Dynamics of Glomerular Ultrafiltration in the Rat V. RESPONSE TO ISCHEMIC INJURY

Renal Micropuncture Techniques

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