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J Schnermann

Publications and source records attributed to J Schnermann.

At least 127 records · Page 7Linked to original sources
PubMed1975

The hydraulic conductivity of the rat proximal tubular wall determined with colloidal solutions.

The hydraulic conductivity of the rat proximal tubular wall was determined using colloidal solutions perfused in short (50--200 mum) (SMP) or long (90--200 mum) (LMP) proximal tubular segments. In SMP human serum albumin (HSA) or polyvinylpyrrolidone (PVP) was added to raffinose solutions. A Lp of 0.019 nl-min-1-mm-1-mm Hg-1 was found when high colloid concentrations were used while values of 0.055--0.092 were found when low colloid concentrations were used. In other experiments, the Lp was determined by perfusing short tubular segments with pure raffinose solutions. A value of 0.015 nl-min-1-mm-1-mm Hg-1 was found. This is twice the value found when raffinose solutions were perfused through long tubular segments and it is concluded that the short microperfusion technique overestimates Lp with a factor of two. When microperfusions of long tubular segments were conducted, PVP was added to an equilibrium solution consisting of NaCl (110 mM) and raffinose (80 mM). Lp was found to be 0.018--0.021 when high colloid concentrations were used, while a value of 0.029 was found when a low colloid concentration was used. As found in both SMP and LMP a decrease in Lp's with increasing colloid concentrations indicates that a significant influence of radial concentration differences is highly probable. It is therefore suggested that the highest Lp derived when using the lowest colloid concentrations represents the best estimate. With this Lp value (0.03--0.05 nl-min-1-mm-1-mm Hg-1) and the existing transtubular hydrostatic and oncotic pressure difference it can be calculated that these passive forces might constitute the driving force for 1/3 of the fluid reabsorbed in the proximal tubule.

Animals↗
PubMed1975

Maintenance of feedback regulation of filtration dynamics in the absence of divalent cations in the lumen of the distal tubule.

In the present experiments we have studied the hypothesis that the feedback responses of glomerular capillary pressure and glomerular filtration rate to elevated distal fluid delivery depend to some extent on the luminal concentration of calcium or magnesium [1]. Loops of Henle were therefore perfused with the following solutions which were designed to yield wide variations of distal divalent cation concentration: 1. Ringer, 2. 140mM NaCl, 3. 125mM NaCl + 10mM CaCl2, 4. 125 mM NaCl + 10 mM MgCl2, 5. 125 mM NaCl + 10 mM Na citrate, and 6. 125 mM NaCl + 10 mM EDTA. During orthograde perfusion with these solutions stop flow pressure (SEP) and early proximal flow rate (EPFR) were measured in each nephron at perfusion rates of 0, 15, 30, and 45 nl/min. We found that perfusion with solutions 2 to 6 did not significantly modify the flow induced change of SFP or EPFR observed during Ringer perfusion. To expose the macula densa cells to chemically well defined solutions loops of Henle were retrogradely perfused from the distal tubule and EPFR was measured in a given nephron with and without perfusion. Identical reductions of EPFR were induced by retrograde perfusions with 140 mM NaCl, 125 mM NaCl + 10 mM CaCl2, and 125 mM NaCl + 10 mM EDTA. Furthermore, an almost complete blunting of the feedback response was noted during retrograde perfusion with 25 mM NaCl. Addition of 5 mM CaCl2 failed to restore the feedback reaction. These results do not support the concept that luminal divalent cations participate in the initiation of tubulo-glomerular feedback responses.

Animals↗
PubMed1975

Impaired potency for feedback regulation of glomerular filtration rate in DOCA escaped rats.

The present experiments were performed to study the effect of chronic extracellular volume expansion on the magnitude of tubulo-glomerular feedback responses in the rat kidney. Extracellular volume expansion was achieved by giving isotonic saline as drinking water and by injecting DOCA in a dose of 2.5 mg/kg - day. When Ringer perfusion rate through the loop of Henle was elevated in control rats (receiving only saline as drinking water) stop flow pressure (SFP) fell by an average of 0.47 +/- 0.81 mm Hg (mean +/- S.D.) and 7.93 +/- 2.85 mm Hg at the flow rate steps of 0--15 nl/min and 15--40 nl/min respectively. SN-GFR was reduced by a mean of 1.3 +/- 0.97 nl/min (0--15 nl/min) and 10.3 +/- 2.45 nl/min (15--40 nl/min). In DOCA treated rats the mean reductions of SFP were 0.98 +/- 0.9 mmHg and 2.1 +/- 1.4 mmHg and of SN-GFR 0.06 +/- 1.8 nl/min and 1.94 +/- 2.3 nl/min. Thus, significantly smaller changes of both SFP and SN-GFR were found in DOCA treated animals when flow rate was elevated from 15--40 nl/min. Net loop NaCl absorption rates did not significantly differ between control and DOCA rats. Renin activity of 5 pooled microdissected glomeruli was 15.6 +/- 17.1 ng/hr-0.1 ml in control and 2.94 +/- 2.6 ng/hr-0.1 ml in DOCA treated rats (P less than 0.01). It is possible therefore that the reduced feedback reactivity in DOCA treated rats is related to the diminished juxtaglomerular renin activity.

Animals↗
PubMed1974

Interference with feedback control of glomerular filtration rate by furosemide, triflocin, and cyanide.

Microperfusion experiments have shown that increases in flow rate of tubule fluid through the loop of Henle are followed by reductions in single nephron glomerular filtration rate (SNGFR) and stop-flow pressure (SFP) measured in the proximal tubule of the same nephron. Because changes in luminal sodium concentration are not consistently related to changes in SNGFR and SFP, we explored the possibility that a transport step at a flow-dependent distal-sensing site might be involved in feedback control of SNGFR. Because the macula densa cells of the distal tubule are adjacent to the glomerular vessels of the same nephrons, they could be the distal-sensing mechanism. We perfused superficial loops of Henle from late proximal to early distal segments in three groups of rats while measuring SFP in the proximal tubule of the same nephron, SNGFR in the proximal tubule of the same nephron, or flow rates of fluid, Na, K, and Cl emerging from the perfused loops. Perfusion solutions used were 0.15 NaCl, Ringer or Ringer with one of several inhibitors of electrolyte transport. Perfusion rates were 10 or 40 nl/min (also, zero during measurements of SFP and SNGFR). With Ringer alone the loop-flow rate increased from 10 to 40 nl/min, caused a decrease in SFP from 37.6 to 32.1 mm Hg, and a decrease in SNGFR from 29.9 to 18.7 nl/min. Concentrations of Na, K, and Cl in early distal fluid and absorption of Na and Cl along the loop segment were also increased when loop perfusion rate was increased. Decreasing the perfusion rate to zero had little effect on SFP or SNGFR. The SFP response to increased flow rate did not occur when the perfusion solution contained furosemide (10(-4) M). No reduction of the SFP response was seen with other diuretics tested (amiloride, acetazolamide, ethacrynic acid, mercaptomerin) or with 0.15 M NaCl alone. The SNGFR response to increased perfusion rate was reduced by furosemide, triflocin, and cyanide but not by amiloride. Na and Cl absorption by the perfused segment were inhibited by furosemide, triflocin, cyanide, and amiloride. Amiloride and acetazolamide, probably do not act in the ascending limb. Ethacrynic acid and mercaptomerin are known to be ineffective in rat nephrons. Thus, agents that could have inhibited NaCl absorption by macula densa cells interfered with the feedback mechanism.

Acetazolamide↗
PubMed1973

Tubuloglomerular feedback. Nonlinear relation between glomerular hydrostatic pressure and loop of henle perfusion rate.

The present experiments were performed to quantify the effect of changes in distal tubular sodium delivery on glomerular flow dynamics both below and above the normal physiologic range. Glomerular capillary pressure as derived from the tubular stop flow pressure was assessed while the loop of Henle of the same nephron was perfused with varying flow rates. During Ringer perfusion no change of glomerular capillary pressure was observed when flow was increased from 0 to 13 nl/min. Further increasing flow to 27 nl/min was associated with a reduction of glomerular hydrostatic pressure by an average of 7.0+/-4.4 cm H(2)O (+/-SD). During perfusion at a rate of 43 nl/min glomerular pressure was decreased by a mean of 10.5+/-4.0 cm H(2)O. Changing the flow rate in small steps revealed that a significant reduction of capillary pressure was found when increasing the flow rate from 13 to 21 nl/min and that the maximum response was reached at 32 nl/min. No effect of perfusion rate changes on glomerular capillary pressure was observed when 300 mM mannitol was used as perfusion fluid. These results imply that a nonlinear relationship exists between end-proximal flow rate and glomerular capillary pressure. It is suggested that during deviations of distal sodium delivery into a positive direction filtration rate is intrarenally regulated probably by prevalence of afferent arteriolar constriction. During reductions of distal sodium load intrarenal regulation is either abolished or it involves proportionate resistance changes of both afferent and efferent arterioles.

Animals↗