Filtration in surface glomeruli as regulated by flow rate through the loop of henle

Hierholzer, Klaus; Müller-Suur, R; Gutsche, Hans-Ulrich; Butz, M.; Lichtenstein, I.

doi:10.1007/bf00585685

Cited by 44 publications

(11 citation statements)

References 31 publications

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“…In contrast, during volume expansion the GFR is high, and a large load of fluid is passing through the whole nephron (Persson, Schnerman & Wright 1974, Ploth et al 1978, Moore et al 1980. The existence of a tubuloglomerular feedback control that can adjust the GFR in accordance with the distal delivery of fluid has been well documented (Schnermann, Persson & Agerup 1973, Hierholzer et al 1974. In earlier studies it was found that the sensitvity of the tubuloglomerular feedback mechanism was reduced during saline volume expansion and plasma volume expansion, allowing more fluid to pass through the distal tubule without reducing the GFR (Persson, Schnermann & Wright 1974, Ploth et al 1978, Moore et al 1980.…”

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confidence: 99%

Activation of the tubuloglomerular feedback mechanism in dehydrated rats

Selén

Müller-Suur

Persson

1983

Acta Physiologica Scandinavica

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To study the influence of the tubuloglomerular feedback control (TGF) on the regulation of glomerular filtration rate (GFR) during dehydration, micropuncture experiments were performed on surface nephrons of dehydrated rats. Dehydration was achieved by withdrawal of food and water for 24 h. The urine flow rate decreased to 1.5 microliters/min (controls 2.9 microliters/min) and GFR decreased in these rats to 0.80 ml/min (controls 1.22). TGF was studied by two different micropuncture procedures. With the first technique the changes in proximal stop-flow pressure in response to changes of the late proximal microperfusion rate were measured. With this technique the perfusion rate necessary to induce a half maximal stop-flow pressure response, the turning point, was also determined. An increased TGF sensitivity was found in dehydrated rats, as indicated by increased stop-flow pressure responses (35 versus 26%) and decreased turning points (16 versus 21 nl/min). With the second micropuncture technique the single nephron GFR (SNGFR) was measured at distal and proximal tubular sites, in the same nephron. Distal SNGFR was decreased during dehydration to 32.2 nl/min, versus 42.7 nl/min in controls. A significant difference between paired SNGFR measurements in the same nephron was observed during dehydration, the proximal value being 5.3 nl/min higher than the distal, whereas this difference was not seen in control rats. This finding indicates that activation of the feedback mechanism takes place to reduce SNGFR. It is concluded that the decrease in whole kidney GFR is partly caused by the observed increase in feedback activity. The present results are also in agreement with our earlier hypothesis that the hydrostatic and oncotic pressure conditions within the interstitial space surrounding the macula densa cells modulate the sensitivity of the tubuloglomerular feedback mechanism.

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mentioning

confidence: 99%

Activation of the tubuloglomerular feedback mechanism in dehydrated rats

Selén

Müller-Suur

Persson

1983

Acta Physiologica Scandinavica

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“…Simi larly, Maddox et al [22] found no difference between snGFR measured at proximal and distal sites using the conventional technique in either uninephrectomized plasma-loaded rats or in normal hyropenic rats. In contrast, Hierholzer et al [2] reported that snGFRprox increased when the loop of Henle was not perfused. However, the difference between snGFR measured with and without loop per fusion was statistically significant only when it was factored by whole kidney GFR and body weight.…”

Section: Discussionmentioning

confidence: 89%

“…The prediction that snGFRprox exceeds snGFRdis as determined using conventional techniques has received a great deal of atten tion [1][2][3][4][5][6][7][8][9][10][11][12][19][20][21][22][23]. Intratubular injection of a column of oil at the puncture site interrupts flow distally.…”

Section: Discussionmentioning

confidence: 99%

“…It has been proposed that a decreased flow of tubular fluid in the macula densa segment inhibits the release of renin and that this initiates a sequence of events leading to an increased glomerular filtration rate [1][2][3][4][5][6][7][8][9][10][11][12][13][14], The conventional technique for measuring single nephron glomerular filtration rate (snGFR) consists of injecting an oil block into a tubule, then quantitatively collecting fluid proximal to the block. If the tubuloglomerular feedback system described above operates, snGFR measured at proximal tubu lar sites (snGFRprox) should consistently ex ceed that measured at distal tubular sites (snGFRdis) because flow of tubular fluid ceases distal to the oil block.…”

Section: Introductionmentioning

confidence: 99%

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Tubulo-Glomerular Feedback in the Rat

Churchill

McDonald

1977

Nephron

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Using conventional micropuncture techniques in 53 adult Sprague-Dawley rats anesthetized with sodium pentobarbital, single nephron GFR at proximal sites (snGFR_prox) averaged 30 ± 1 nl/min (76 tubules) and at distal sites (snGFR_diS), 33 ± 2 nl/min (90 tubules). Thus, in spite of interruption of macula densa fluid flow during its measurement, snGFR_proX was not significantly greater than snGFR_diS (p > 0.05). Whole kidney GFR averaged 0.9 ± 0.07 ml/min before and 1.0 ± 0.05 ml/min during an intravenous infusion of SQ20,881, a substance which inhibits production of angiotensin II. Similarly, snGFR_diS was unaffected by SQ20,881; the mean difference between paired snGFRdis (collection during NaCl infusion minus recollection at same sites during SQ20,881 infusion) was 6 ± 4 nl/min (p > 0.5). These results suggest that under the conditions of the experiments, tubulo-glomerular feedback is not operative and that angiotensin II plays no role in controlling filtration.

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“…The specific changes in the individual determinants of SNGFR [nephron plasma flow (SNPF), transcapillary hydrostatic pressure gradient (AP), glomerular ultrafiltration coeffi cient (LpA), and systemic plasma oncotic pressure (tca)] responsible for the decline in nephron filtration rate associated with TGF have been evaluated by a number of investigators. Despite some discordance among the results of the various studies pertaining to this matter, evidence has accrued to implicate both afferent and efferent arteriolar vasoconstriction [20][21][22][23] as well as decline in LpA [22,24] in the glomerular response to perfusion of the macula densa. It has also been demon strated that angiotensin II (All), a hormone capable of mediating efferent arteriolar vasoconstriction and de creases in L.pA (presumably by causing mesangial cells to contract) [25], must be present in renal tissue in order for a TGF response to occur [26,27], suggesting that the intrarenal concentration of, or the glomerular sensitivity to All might be modulated by the TGF system.…”

Section: The Tgf Mechanismmentioning

confidence: 99%