Feedback pressure-flow responses in normal and angiotensin-prostaglandin-blocked rats

Persson, A. Erik G.; Gushwa, Leslie C.; Blantz, Roland C.

doi:10.1152/ajprenal.1984.247.6.f925

Cited by 26 publications

(23 citation statements)

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“…Since changes in the Pg, on maximal activation or inactivation of TGF are known (Persson, Gushwa & Blantz, 1984) and since it is also known that even under such conditions, renal autoregulation is preserved, for instance during the administration of acetazolamide or furosemide (Duchin, Peterson & Burke, 1977), the values for the different resistances can be calculated.…”

Section: R4mentioning

confidence: 99%

Increased tubuloglomerular feed‐back mediated suppression of glomerular filtration during acute volume expansion in rats.

Davis¹,

Häberle²,

Kawata³

et al. 1988

The Journal of Physiology

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SUMMARY1. Volume expansion is currently believed to change the intrinsic properties of the juxtaglomerular apparatus such that the sensitivity of the tubuloglomerular feedback (TGF) mechanism is reduced, thus allowing glomerular filtration rate, and hence salt and water excretion, to rise. Recent studies conflict with this view and indeed the older literature reveals that the rise in glomerular filtration rate (GFR) under these conditions is far more modest than would be expected if TGF control were eliminated.2. To investigate this problem, TGF control of filtration rate was examined by measuring single-nephron glomerular filtration rate (SNGFR) during loop of Henle perfusion at varying rates in rats under control conditions, after acute, moderate (4% of body weight), iso-oncotic volume expansion and in rats treated with antibodies to atrial natriuretic peptide (ANP) prior to the acute volume expansion.3. With TGF control of filtration interrupted by filtrate collection from the proximal tubule, SNGFR in the expanded rats was massively increased compared with controls, although SNGFR measured in the distal tubule, and hence with TGF control intact, was only modestly increased, as was whole-kidney filtration rate.Loop perfusion at increasing rates up to 30 nl min-' progressively decreased SNGFR in controls, and in the expanded rats the range over which control was exerted extended up to 60-80 nl min-'. For changes in loop flow around the spontaneous operating point, the sensitivity of the TGF mechanism, defined as A SNGFR/A loop flow, was similar in both groups. Treatment of rats with ANP antibodies prior to volume expansion substantially blunted the changes in renal salt and water excretion and the increase in SNGFR seen in the absence of loop perfusion.4. These results are not consistent with a diminution of TGF function after

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Section: R4mentioning

confidence: 99%

Increased tubuloglomerular feed‐back mediated suppression of glomerular filtration during acute volume expansion in rats.

Davis¹,

Häberle²,

Kawata³

et al. 1988

The Journal of Physiology

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“…Indo inhibits cyclooxygenase and reduces the production of all PGs including PGI2 and TX (4,6,7). Indo (2.5 mg -ml-', Sigma Chemical Co.) was dissolved in 1 M Na2CO3 solution and given to group 2 rats to assess the effects of nonselective inhibition of production ofboth vasodilator and vasoconstrictor PGs on the TGF response.…”

Section: Introductionmentioning

confidence: 99%

Modulating role for thromboxane in the tubuloglomerular feedback response in the rat.

Welch

Wilcox²

1988

J. Clin. Invest.

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Sbme studies have indicated that PGs can modulate the single nephron tubuloglomerular feedback (TGF) response. The aim of this study was to define the specific role of the vasoconstrictor PG, TX, by administration to rats of either vehicle (group 1; n = 20) or drugs that inhibit either cyclooxygenase (indomethacin lindol, 5 mg * kg-', group 2, n = 17), TX synthetase 485 [UK], 100 mg kg-', group 3, n = 19), or TX receptors 548 [SQJ, group 4, n = 14,953 [L, 50 mg. kg-', group 5, n = 8). Indo reduced excretion of the prostacyclin derivative 6-keto-PGF14, and TXB2 and lowered whole kidney GFR and renal plasma flow, whereas UK lowered excretion of TXB2 only and did not change basal renal hemodynamics. The TGF response (assessed from reduction in proximal tubule stop-flow pressure (Pf, mmHg) during increases in perfusion of the loop of Henle (LH) from 0 to 40 nl* min-') was unchanged after vehicle (9.8±0.5-10.9±1.0, NS) but blunted (P < 0.001) by 40-65% in rats of groups 2-5 (indo, 11.1±1.0-4.4±0.7; UK, 9.0±0.8-4.8±0.7; SQ, 10.3±0.6-4.8±0.6; L, 10.7±0.5-6.7±13). This blunting was due to lower values for Pdf at zero LH flow after indo, SQ, and L, and higher values of Pf at 40 nl. min'1 LH flow after indo and UK. The fall in single nephron GFR (SNGFR, nl min-1) with increasing LH perfusion was unchanged after vehicle (10.9±2.8-11.2±0.8) but was blunted (P < 0.05) by 45-55% in rats given indo (13.9±1.2-6.2±2.2) or UK (12.8±2.1-7.0±1.5). UK produced dose-dependent reductions in TXB2 excretion (IC50, 15 mg * kg-lJ and inhibition of the TGF response (IC5o: 30 mg-kg-'). After blockade of TX receptors by SQ, UK had no further affect on the TGF response. The fall in Pf at high LH flow was blunted (P < 0.05) by indo and UK, whereas the rise in Pf at zero LH flow was blunted by indo, SQ, and L.

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“…A similar efficacy test has recently been used successfully in studies designed to determine the role of P2 receptors in renal blood flow autoregulation (21). We do not think that the nearly exclusive reliance on P SF measurements to assess TGF responsiveness limits the strength of our conclusions to a major extent, although a dissociation between P SF and SNGFR responses over the entire relevant range of tubular flows has been observed under conditions of simultaneous cyclooxygenase and ACE inhibition (22). In this rare and singular case, P SF responses were found to be absent while SNGFR responses were partially maintained.…”

Section: Discussionmentioning

confidence: 74%

Maintained tubuloglomerular feedback responses during acute inhibition of P2 purinergic receptors in mice

Schnermann

2011

American Journal of Physiology-Renal Physiology

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lar feedback (TGF), the change of afferent arteriolar resistance initiated by changes of luminal NaCl concentration, is thought to be related to NaCl-dependent release of ATP by macula densa cells. In the present study, we have explored the possibility that the released ATP may directly interact with vasoconstrictor P2 purinergic receptors in the vicinity of the glomerular vascular pole. In two different strains of wild-type mice (SWR/J and FVB), TGF responses were determined in vivo by measuring the stop flow pressure (PSF) change caused by a saturating increase in loop of Henle flow rate before and during the administration of the P2 receptor inhibitors PPADS (12 mg/kg ϩ 35 mg·kg Ϫ1 ·h Ϫ1 iv) or suramin (50 mg/kg ϩ 150 mg·kg Ϫ1 ·h Ϫ1 ). Both agents significantly reduced the blood pressure response to the P2X agonist ␣,␤-methylene ATP. In SWR/J and FVB mice, elevating flow to 30 nl/min reduced PSF by 16.4 Ϯ 2.2 and 17.1 Ϯ 1.8%. During infusion of PPADS, PSF fell by 18.8 Ϯ 2 (P ϭ 0.4) and 16.5 Ϯ 1.5% (P ϭ 0.82) in the two strains of mice. During suramin infusion, PSF decreased by 14.7 Ϯ 2.4 (P ϭ 0.62) and 15 Ϯ 1.3% (P ϭ 0.4) in SWR/J and FVB mice, respectively. Including PPADS (10 Ϫ4 M) in the loop perfusate did not significantly alter the PSF response (18.9 Ϯ 1.8%; P ϭ 0.54). Arterial blood pressure was not systematically affected by the P2 inhibitors. As measured by free-flow micropuncture, PPADS significantly reduced proximal tubular fluid reabsorption in both fractional and absolute terms. These results indicate that the direct activation of P2 purinergic receptors by ATP is not a major cause of TGF-induced vasoconstriction in vivo.PPADS; suramin; stop-flow pressure; proximal reabsorption; micropuncture THE TUBULOGLOMERULAR FEEDBACK (TGF) response is defined as the change in glomerular filtration rate or glomerular capillary pressure when the perfusion rate in the loop of Henle of individual nephrons is altered (26). There is general agreement that this response is for the most part the result of a direct relationship between the loop of Henle perfusion rate and afferent arteriolar resistance. In addition, experimental evidence favors the notion that TGF-dependent vasomotion is initiated by purinergic control mechanisms activated by the flow-dependent release of ATP from macula densa cells into the underlying extraglomerular mesangial interstitium (3). It has remained uncertain how any released ATP may affect the tone of the afferent arterioles.One proposal has been that ATP activates P2 receptors on extraglomerular mesangial cells and that the resulting increase in cytosolic Ca is transmitted to the afferent arteriole through gap junctional coupling (14,19). ATP may also directly activate P2 receptors on the afferent arteriole, with P2X1 receptors being the most likely receptor subtype since its presence in afferent arterioles has been well documented (8). Alternatively, ATP may be dephosphorylated to AMP and adenosine by ecto-ATPases and ecto-5= nucleotidase, a paradigm that has been shown to underlie the ...

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Feedback pressure-flow responses in normal and angiotensin-prostaglandin-blocked rats

Cited by 26 publications

References 0 publications

Increased tubuloglomerular feed‐back mediated suppression of glomerular filtration during acute volume expansion in rats.

Increased tubuloglomerular feed‐back mediated suppression of glomerular filtration during acute volume expansion in rats.

Modulating role for thromboxane in the tubuloglomerular feedback response in the rat.

Maintained tubuloglomerular feedback responses during acute inhibition of P2 purinergic receptors in mice

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