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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 1245-1248 
    ISSN: 1432-1440
    Keywords: Chronic salt loading ; Volume expansion ; Glomerular filtration rate ; Tubuloglomerular feedback ; Humoral substances in tubular fluid ; Chronische Salzbelastung ; Volumenexpansion ; Glomeruläre Filtrationsrate ; Tubuloglomeruläre Rückkoppelung ; Humorale Substanzen in tubulärer Flüssigkeit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei normalem Extrazellulärvolumen reduziert der Harnfluß durch das macula densa Segment der Henle'schen Schleife die glomeruläre Filtrationsrate durch ein Signal aus dem juxtaglomerulären Apparat (tubuloglomerulärer Rückkopplungsmechanismus, TGF). Bei Vergrößerung des Extrazellulärvolumens wird dieser Mechanismus gehemmt, so daß die glomeruläre Filtrationsrate ansteigt. Um festzustellen, ob diese Hemmung durch Veränderungen im juxtaglomerulären Apparat oder in der Tubulusflüssigkeit verursacht wird, wurden an zwei Gruppen von Ratten, deren Extrazellulärvolumen entweder normal war oder durch kochsalzreiche Ernährung expandiert wurde, Austauschversuche mit spätproximaler Tubulusflüssigkeit durchgeführt. Die Tubulusflüssigkeit wurde mit Mikrosaug/Perfusionspumpen gesammelt. Ihre Wirkung auf den TGF wurde geschätzt, indem Henle'sche Schleifen einzelner Tubuli mit 40, 10, und 0 nl/min perfundiert wurden, während gleichzeitig der Harnfluß (EPF) in einem glomerulusnahen Segment des jeweiligen proximalen Tubulus gemessen wurde. Insalzreich ernährten Tieren war die EPF von der Schleifenperfusionsrate unabhängig, wenn die Henle'schen Schleifen mithomologer Tubulusflüssigkeit perfundiert wurden. Mit Tubulusflüssigkeit aussalzarm ernährten Tieren und einer Schleifenperfusionsrate von 40 nl/min fiel die EPF jedoch um etwa 50% gegenüber dem Kontrollwert bei nichtperfundierter Schleife ab. Insalzarm ernährten Tieren, deren Henle'sche Schleifen mithomologer Tubulusflüssigkeit und einer Rate von 40 nl/min perfundiert wurden, fiel die EPF um etwa 50% gegenüber dem Kontrollwert bei nicht perfundierter Schleife ab. Mit Tubulusflüssigkeit aussalzreich ernährten Tieren war die EPF von der Schleifenperfusionsrate unabhängig. Es wird gefolgert, daß der TGF in volumenexpandierten Tieren durch eine Substanz in der Tubulusflüssigkeit gehemmt wird.
    Notes: Summary Experiments were carried out in Wistar rats to determine whether the loss of sensitivity of the tubuloglomerular feedback mechanism (TGF) which is known to occur in volume expansion is due to a change in the functional characteristics of the juxtaglomerular apparatus or to a change in some property of the tubular fluid which influences the feedback signal at the macula densa. Proximal tubular fluid was collected by means of a microperfusion/suction pump from Wistar rats maintained for a minimum of 10 days on a high salt diet and also from rats fed a control low salt diet. Both fluids were then used to perfuse loops of Henle in rats from both groups and the feedback response assessed from the change in early proximal tubular flow rate (EPF). In high salt rats, perfusion of the loop of Henle with homologous tubular fluid confirmed the loss of sensitivity of the TGF mechanism in volume expansion, the response of EPF was practically absent. In contrast, the low salt rat responded with a 50% decrease in EPF to loop perfusion at 40 nl/min with its homologous fluid. On the other hand, when the loop of Henle in high salt rats was perfused at 40 nl/min with heterologous (low salt) tubular fluid, EPF again decreased by some 50% whereas EPF in low salt rats failed to respond to loop perfusion with high salt fluid. From these results it is concluded that in rats chronically volume expanded by a high salt diet an unknown inhibitory principle occurs in the proximal tubular fluid which reduces the sensitivity of the tubuloglomerular feedback mechanism.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 411 (1988), S. 322-327 
    ISSN: 1432-2013
    Keywords: Tubuloglomerular feedback ; Juxtaglomerular apparatus ; Glomerular filtration rate ; Acute volume expansion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Loss of sensitivity or “resetting” of tubuloglomerular feedback has been reported after both acute and chronic volume expansion in rats. In chronic volume expansion due to dietary salt loading, resetting was found to result from the appearance of an inhibitory factor in tubular fluid. The aim of the present study was to test the possibility that resetting after acute isooncotic volume expansion may also be due to such an inhibitor. Rats were acutely volume expanded (4.5% of body weight) by infusion of a solution of fresh plasma and Ringer's solution. Tubuloglomerular feedback activity was assessed in expanded and control animals by measuring early proximal flow (EPF) rate during perfusion of the loop of Henle at varying rates with proximal tubular fluid harvested from the control (control TF) and expanded animals (AVE TF). When loops of Henle in control animals were perfused with control TF at 10, 20 or 40 nl min−1, EPF fell from (mean ±SD) 29.8±5.6 at zero loop flow to 27.5±7.5, 21.1±4.2 and 15.5±4.5 nl min−1 gKW−1 respectively. Perfusion at the same rates with control TF in expanded animals reduced EPF from 39.5±9.6 (at zero loop flow) to 35.9±11.3, 31.6±4.3 and 22.9±6.8 nl min−1 gKW−1 respectively. When loops of Henle in control animals were perfused with AVE TF, EPF fell from 28.6±9.5 (zero loop flow) to 23.5±8.6, 19.9±8.2 and 15.6±6.5 nl min−1 gKW−1 respectively. Perfusion at these rates with AVE TF in the expanded animals depressed EPF from 36.7±7.8 (at zero loop flow) to 33.6±7.3, 28.6±7.6 and 22.7±8.0 nl min−1 gKW−1 respectively. Since the responses to the two perfusion fluids were the same in each group, it is concluded that there is no inhibitory factor present in AVE TF. Although EPF at each perfusion rate was significantly higher in the expanded animals than in control, the change in EPF per unit change in loop perfusion rate was the same in both groups from which it is concluded that no resetting of tubuloglomerular feedback occurred in the present study.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2013
    Keywords: Autoregulation ; Tubuloglomerular feedback ; Renal blood flow ; Glomerular filtration rate ; Plasma renin activity ; Deoxycorticosterone acetate ; Plasma volume ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tubuloglomerular feedback (TGF) function and autoregulation (renal blood flow RBF; glomerular filtration rate, GFR; single-nephron glomerular filtration rate, SNGFR) were examined in rats chronically treated with deoxycorticosterone acetate (DOCA) and given isotonic saline to drink. DOCA treatment depressed arterial plasma renin activity, expanded plasma volume by 25% and increased arterial blood pressure. Autoregulation of RBF and GFR was maintained in the DOCA animals above 90 mm Hg and 110 mm Hg respectively, whereby both GFR and RBF were lower than in controls. Micropuncture experiments demonstrated the absence of TGF in the DOCA animals. There was no difference between SNGFR values measured in the distal and proximal tubules, nor was there a significant response of SNGFR when loops of Henle were perfused with Ringer's solution at 20 nl/min. Loop perfusion in control rats with tubular fluid collected in DOCA rats elicited a normal TGF response, showing that TGF inhibition in the DOCA animals is due to changes in the function of the juxtaglomerular apparatus. In contrast to control rats, proximal SNGFR was perfectly autoregulated. These results suggest that TGF is not primarily responsible for autoregulation and that the vasodilatation normally resulting from acute TGF interruption is therefore compensated by some other mechanism such that RBF and GFR are lower than in controls.
    Type of Medium: Electronic Resource
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