Failure of tubule fluid osmolarity to affect feedback regulation of glomerular filtration

1980 ◽  
Vol 239 (5) ◽  
pp. F427-F432 ◽  
Author(s):  
J. P. Briggs ◽  
J. Schnermann ◽  
F. S. Wright
Keyword(s):  
Flow Rate ◽  
Feedback Regulation ◽  
Solute Concentration ◽  
Tubuloglomerular Feedback ◽  
Sprague Dawley ◽  
Perfusion Flow ◽  
Sprague Dawley Rats ◽  
Nacl Concentration ◽  
Osmotic Agents ◽  
Feedback Responses

Experiments were performed in Sprague-Dawley rats in order to distinguish between sodium chloride and total solute concentration as possible luminal signals capable of eliciting tubuloglomerular feedback responses. Early proximal flow rate (VEP), an index of nephron filtration rate, was measured without perfusion of the loop of Henle and during retrograde perfusion with solutions containing 20, 35, 60 to 100 mM NaCl and varying amounts of either urea or mannitol to achieve total solute concentrations of 130, 280, or 400 mosM. Perfusion flow rate was kept constant at 20 nl/min. Perfusion with a solution containing 20 mM NaCl and made hypo-, iso-, or hypertonic with urea or mannitol caused little or no change in VEP. Perfusion with a 35 mM NaCl solution made hypo-, iso-, or hypertonic with mannitol resulted in a fall of VEP of 6-7 nl/min. When NaCl concentration was 60 mM, VEP fell by 10-14 nl/min with solutions made hypo-, iso-, or hypertonic with urea or mannitol. With 100 mM NaCl solutions made hypo-, iso-, or hypertonic with mannitol, VEP fell approximately 12 nl/min. These results indicate that feedback responses are determined by the NaCl concentration of the perfusate and that this NaCl dependency is not modified by varying perfusate osmolarity between 130 and 400 mosM with urea or mannitol as osmotic agents.

scholarly journals Tubuloglomerular feedback in Dahl rats

1998 ◽  
Vol 274 (6) ◽  
pp. R1561-R1569 ◽  
Author(s):  
Finn M. Karlsen ◽  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou
Keyword(s):  
Flow Rate ◽  
Tubuloglomerular Feedback ◽  
Sprague Dawley ◽  
Compensatory Response ◽  
High Salt Diet ◽  
Salt Diet ◽  
Sprague Dawley Rats ◽  
Intratubular Pressure ◽  
Low Salt ◽  
Experimental Rat Model

We have previously demonstrated a loss of autoregulation in Dahl salt-sensitive (Dahl-S) rats rendered hypertensive on a high-salt diet. To determine whether this was due to a decreased activity of either the myogenic or the tubuloglomerular feedback (TGF) response, we tested the TGF response in both Dahl-S and salt-resistant Dahl rats on high- and low-salt diets. TGF was investigated in the closed-loop mode with a videometric technique, in which the response in late proximal flow rate to perturbations in Henle flow rate was measured. All Dahl rats showed a similar compensatory response to perturbations around the natural operating point, with a TGF response that was more efficient than in normotensive Sprague-Dawley rats. No evidence of decreased TGF responsiveness in hypertensive Dahl-S rats was found. The results suggest that the loss of autoregulation in hypertensive Dahl-S rats is due to a compromised myogenic response. We also measured the free-flow proximal intratubular pressure in Dahl rats. Perfectly regular oscillations were demonstrated in all Dahl series, including the hypertensive Dahl-S rats. This is the first demonstration of regular oscillations in an experimental rat model of hypertension.

Oscillations of tubular pressure, flow, and distal chloride concentration in rats

1989 ◽  
Vol 256 (6) ◽  
pp. F1007-F1014 ◽  
Author(s):  
N. H. Holstein-Rathlou ◽  
D. J. Marsh
Keyword(s):  
Flow Rate ◽  
Fluid Velocity ◽  
Chloride Concentration ◽  
Feedback Mechanism ◽  
Tubuloglomerular Feedback ◽  
Sprague Dawley ◽  
Mean Values ◽  
Sprague Dawley Rats ◽  
Proximal Tubular ◽  
Chloride Activity

Previous experiments have shown oscillations in proximal tubular pressure in halothane-anesthetized rats. Such oscillations should be due to oscillations in flow rate and should cause periodic oscillations in both distal tubular chloride concentration and distal tubular pressure. The purpose of the study was to test these predictions. In halothane-anesthetized Sprague-Dawley rats, distal tubular chloride activity was measured with Cl- -sensitive electrodes, and late proximal flow rate was measured by pulse injection of boluses of solutions containing rhodamine dextran. Bolus velocity was detected by videomicroscopy. The time resolution was 2 s. All four variables oscillated with the same frequency, approximately 35 mHz. The amplitude of the flow and the chloride oscillations were 28 and 10%, respectively, of the mean values. Proximal fluid velocity led proximal pressure by 1.5 +/- 0.4 s, whereas distal chloride activity lagged proximal pressure by 8.9 +/- 0.8 s. The distal pressure lagged the proximal pressure by 1.05 +/- 0.38 s. It is concluded that there is a significant variation in distal chloride activity, the magnitude of which appears to be sufficient to account for the observed flow variations through the operation of the tubuloglomerular feedback mechanism.

Quantitative characterization of the tubuloglomerular feedback response: effect of growth

1984 ◽  
Vol 247 (5) ◽  
pp. F808-F815 ◽  
Author(s):  
J. P. Briggs ◽  
G. Schubert ◽  
J. Schnermann
Keyword(s):  
Flow Rate ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Sprague Dawley ◽  
Maximum Slope ◽  
Sprague Dawley Rats ◽  
Single Nephron ◽  
Renal Micropuncture ◽  
The Right

Studies were performed to characterize quantitatively the effect of changing loop of Henle flow rate on single nephron glomerular filtration rate (SNGFR) in male Sprague-Dawley rats of varying body weight. Rats weighing 100, 220, and 350 g were studied using standard renal micropuncture techniques. The relationship between loop of Henle flow rate (VLP) and SNGFR was characterized for individual nephrons by multiple determinations of SNGFR during loop perfusion. An inverse sigmoidal relationship was observed that could be described as delta SNGFR = a/(1 + ek(b-VLP], where delta SNGFR is the change in SNGFR from the value measured at zero loop flow, a is delta SNGFRmax, the maximum change, b is V1/2, the flow rate at which the response is half maximum, and k is [4f' (V1/2)]/a with f' (V1/2) the slope at V1/2. delta SNGFRmax increased with increasing body size (7.9 +/- 1.16, 18.9 +/- 0.90, and 25.2 +/- 2.73 nl/min, respectively, in the three groups), and the curve shifted to the right (V1/2 = 10.3 +/- 0.8, 15.4 +/- 0.83, and 22.3 +/- 1.22 nl/min). The maximum slope increased (f' (V1/2) = 0.9 +/- 0.19, 1.7 +/- 0.16, and 3.2 +/- 0.70), but the exponential constant k was uninfluenced by growth. Independent of rat size, a 10% increase in loop flow at the midpoint produced at 5-10% decrease in SNGFR. Free-flow values of SNGFR and VLP were found to lie in the most sensitive range of the feedback curve.

Effect of angiotensin II receptor blockade on proximal tubular fluid reabsorption

1997 ◽  
Vol 273 (2) ◽  
pp. R510-R517 ◽  
Author(s):  
P. P. Leyssac ◽  
F. M. Karlsen ◽  
N. H. Holstein-Rathlou
Keyword(s):  
Angiotensin Ii ◽  
Flow Rate ◽  
Feedback Mechanism ◽  
Tubuloglomerular Feedback ◽  
Sprague Dawley ◽  
Angiotensin Ii Receptor ◽  
Fluid Reabsorption ◽  
Nacl Concentration ◽  
Proximal Tubular ◽  
Tubular Fluid Reabsorption

The effect of physiological concentrations of angiotensin II on proximal tubular fluid reabsorption remains controversial. To investigate the effect of blockade of intratubular AT1 receptors on tubular reabsorption, losartan (10(-5) M) was administered by microperfusion into an early proximal convolution of halothane-anesthetized Sprague-Dawley rats. Four parameters that depend on the rate of proximal fluid reabsorption were measured: proximal intratubular pressure (Pprox), early and late proximal flow rate, and early distal NaCl concentration. Pprox decreased by 0.5 +/- 0.1 mmHg, late proximal flow rate decreased by 2.0 +/- 0.8 nl/min, and early distal NaCl concentration decreased by 4.3 +/- 0.8 mM (mean +/- SE). No changes were observed after microperfusion with saline. Because the tubuloglomerular feedback mechanism was operating in the closed-loop mode, the decreased NaCl load to the macula densa will be compensated by an increase in the single-nephron glomerular filtration rate. In agreement with this, the early proximal flow rate, measured proximal to the site of losartan administration, increased by 5.7 +/- 1.3 nl/min. The increase in the rate of proximal reabsorption between the early and late proximal convolutions was estimated to be 7.8 nl/min (approximately 36%). It is concluded that a decrease in local luminal angiotensin II levels and/or AT1 receptor activity under free flow conditions increases the rate of proximal tubular fluid reabsorption.

Evaluation of prostaglandins as mediators of tubuloglomerular feedback

1988 ◽  
Vol 254 (5) ◽  
pp. F642-F649 ◽  
Author(s):  
M. Franco ◽  
P. D. Bell ◽  
L. G. Navar
Keyword(s):  
Nordihydroguaiaretic Acid ◽  
Tubuloglomerular Feedback ◽  
Hypotonic Solution ◽  
Sprague Dawley ◽  
Lipoxygenase Inhibitor ◽  
Synthesis Inhibitor ◽  
Sprague Dawley Rats ◽  
Rapid Restoration ◽  
Flow Pressure ◽  
Feedback Responses

Orthograde and retrograde microperfusion experiments were conducted in Sprague-Dawley rats to evaluate the participation of vasoconstrictive eicosanoids as mediators of tubuloglomerular feedback (TGF) signals. Retrograde perfusion with 160 microM arachidonic acid (AA) added to a hypotonic solution enhanced the stop-flow pressure (SFP) feedback responses compared with those obtained with the control hypotonic solution (delta SFP, 1.6 +/- 0.4 vs. 10.1 +/- 0.7 mmHg with AA). Blockade of thromboxane A2 (TxA2) with the receptor blocker EP 092 or the synthesis inhibitor UK 38485 did not alter the magnitude of the SFP feedback responses obtained with an isotonic solution. Similarly, nordihydroguaiaretic acid, a lipoxygenase inhibitor, did not alter maximal SFP feedback responses. Although indomethacin (5 mM) did induce attenuated SFP feedback responses (delta SFP, 9.5 +/- 0.7 vs. 0.5 +/- 0.4 mmHg with indomethacin), normal feedback responses were restored within 15-90 s after cessation of indomethacin perfusion. Additionally, SFP feedback responses were not inhibited with 5 mM piroxicam, a different cyclooxygenase inhibitor. These data fail to support a role for either TxA2 or lipoxygenase end products as mediators of TGF signals. The rapid restoration of feedback responses after indomethacin exposure and the lack of blockade with piroxicam suggest that transmission of feedback signals is not dependent on cyclooxygenase products.

Ameliorating effects of cloperastine on dysfunction of the urinary bladder caused by cerebral infarction in conscious rats

2009 ◽  
Vol 87 (11) ◽  
pp. 893-899 ◽  
Author(s):  
Gen Yamamoto ◽  
Fumio Soeda ◽  
Tetsuya Shirasaki ◽  
Kazuo Takahama
Keyword(s):  
Urinary Bladder ◽  
Cerebral Infarction ◽  
Flow Rate ◽  
Bladder Capacity ◽  
Left Middle Cerebral Artery ◽  
Sprague Dawley ◽  
Urinary Bladder Dysfunction ◽  
Sprague Dawley Rats ◽  
Urethral Resistance ◽  
Effective Doses

We investigated the effects of the centrally acting antitussives dextromethorphan and cloperastine on urinary bladder dysfunction 24 h after cerebral infarction in rats using the cystometry technique. First, cystometrography was performed in conscious male Sprague–Dawley rats. Cerebral infarction was then induced by occlusion of the left middle cerebral artery. Twenty-four hours after cerebral infarction, the effect of each drug on micturition disorder was estimated for 5 parameters: bladder capacity, maximum voiding pressure, micturition latency, flow rate, and urethral resistance. Cerebral infarction markedly reduced bladder capacity, micturition latency, and flow rate and increased urethral resistance. After cerebral infarction, intravenous dosing of saline had no effect on these parameters. Dextromethorphan (20 mg/kg) and cloperastine (2.5 and 5.0 mg/kg) at antitussive effective doses significantly increased bladder capacity and micturition latency. Unlike dextromethorphan, cloperastine ameliorated decreases in flow rate and increases in urethral resistance caused by cerebral infarction. These results suggest that cloperastine may have therapeutic value for the treatment of disorders of the micturition reflex associated with cerebral infarction, and that the drug may become a base compound from which to develop more active drugs for such disorders.

Abstract 20074: Hemodynamic Profile of Prolonged Normothermic, Mild Hypothermic, and Deep Hypothermic Emergency Cardiopulmonary Bypass Reperfusion in Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Ingrid A Magnet ◽  
Florian Ettl ◽  
Andreas Schober ◽  
Alexandra-Maria Warenits ◽  
Christoph Testori ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Flow Rate ◽  
Mild Hypothermia ◽  
Temperature Profiles ◽  
Sprague Dawley ◽  
Flow Rates ◽  
Circulating Water ◽  
Sprague Dawley Rats ◽  
Hemodynamic Profile ◽  
75Th Quartile

Background: The hemodynamic profile of rats randomized into prolonged normothermic (NT, 37±0.5°C), mild hypothermic (MH, 33±0.5°C) or deep hypothermic (DH, 27±0.5°C) reperfusion with emergency cardiopulmonary bypass (ECPB), following refractory ventricular fibrillation cardiac arrest (VF CA) was explored. Methods: Fifty adult male Sprague-Dawley rats were put on bypass for 15 min, following 10 min of VF CA. The ECPB setup included a circulating water bath which temperature controlled all animals at target. After 15 min, rats were defibrillated, weaned from bypass, and controlled at 33°C (MH, DH) or 37°C (NT) externally. All rats received a single dose of epinephrine (30 μg/kg), heparin and sodium bicarbonate with the crystalloid priming of the ECPB circuit. ECPB flow rate was kept at 100 mL/kg in all groups. Mean arterial pressure (MAP) was continuously monitored in the femoral artery and is presented as median with 25th/75th quartile mmHg. Results: See figure. There was no difference in MAP before or during CA. For the first 5 min of resuscitation, MAP at a given ECPB flow rate was highest in the DH group (DH 84(69;89), MH 51(49;61), NT 48(37;55) , p = <.001). This was reversed during the last 5 min on bypass (DH 35(30;42), MH 44(37;64), NT 42(33;67), p = .034). For 10 min off bypass, the DH group was relatively hypotensive (DH 46(40;62, MH 64(60;77), NT 61(54;77), p = .005), which was again reversed for the remaining post resuscitation period (DH 68(60;78), MH 59(54;66), NT 53(49;62), p = .008). Conclusions: While the temperature profiles of NT and MH reperfusion were similar, DH caused initially higher pressures followed by a period of hypotension as compared to NT and MH groups at identical epinephrine doses and ECPB flow rates. Off bypass, DH animals were again relatively hypotensive, coinciding with their rewarming to mild hypothermia. Further experiments are needed to determine the cause of this, like hypothermic vasoconstriction, or altered pharmacokinetics.

Mechanism underlying diuretic effect of l-NAME at a subpressor dose

2001 ◽  
Vol 281 (3) ◽  
pp. F414-F419 ◽  
Author(s):  
Mingyu Liang ◽  
Theresa J. Berndt ◽  
Franklyn G. Knox
Keyword(s):  
Proximal Tubule ◽  
Flow Rate ◽  
Nitrate Concentration ◽  
Distal Tubule ◽  
No Synthase ◽  
Urine Flow ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Renal Tubular ◽  
Nitrite Nitrate

The diuretic effects of nitric oxide (NO) synthase inhibitors administered at subpressor dose in rats are controversial, and the tubular segments involved are not known. In the present study, we examined the effect of N ω-nitro-l-arginine methyl ester (l-NAME) at a subpressor dose on renal interstitial NO and cGMP activity and on renal tubular segmental reabsorption of fluid in the rat. Intravenous infusion of l-NAME at 1 μg · kg−1 · min−1 in Sprague-Dawley rats ( N = 8), which did not alter mean arterial pressure or glomerular filtration rate, significantly increased urine flow rate (Uv; from 78.2 ± 12.7 to 117.1 ± 14.9 μl/min, P < 0.05). Paradoxically, this effect of l-NAME was concomitant with significant increases in nitrite/nitrate (from 10.79 ± 1.20 to 16.50 ± 2.60 μM, P < 0.05) and cGMP (from 0.65 ± 0.09 to 0.98 ± 0.18 nM, P < 0.05) concentrations in renal cortical microdialysate as well as the nitrite/nitrate concentration in the medullary microdialysate. Micropuncture studies in the superficial nephron revealed that l-NAME significantly increased the flow rate (from 8.3 ± 0.9 to 12.2 ± 1.2 nl/min, P < 0.05) and fractional delivery of fluid to the distal tubule, but not those in the late proximal tubule. In conclusion, l-NAME, at the subpressor dose used in this study, increased renal nitrate/nitrite and cGMP and inhibited fluid reabsorption in tubular segments between the late proximal tubule and the distal tubule of superficial nephrons.

Resetting of tubuloglomerular feedback: evidence for a humoral factor in tubular fluid

1984 ◽  
Vol 246 (4) ◽  
pp. F495-F500 ◽  
Author(s):  
D. A. Haberle ◽  
J. M. Davis
Keyword(s):  
Flow Rate ◽  
Juxtaglomerular Apparatus ◽  
Ringer Solution ◽  
Humoral Factor ◽  
Inhibitory Factor ◽  
Tubuloglomerular Feedback ◽  
Fluid Composition ◽  
Similar Magnitude ◽  
Feedback Responses

Experiments were performed on chronically salt-loaded rats to determine whether resetting of tubuloglomerular feedback is caused by changes in the sensitivity of the juxtaglomerular apparatus itself or by changes of tubular fluid composition. The feedback response was quantified in both salt-loaded and salt-deplete rats by measuring early proximal flow rate (EPF) during loop perfusion at 40, 10, and 0 nl/min using tubular fluid harvested from both groups and with Ringer solution. In salt-loaded rats endogenous tubular fluid produced only a small feedback response (EPF40-0 = 1.9 +/- 1.5 nl/min), whereas exogenous tubular fluid from salt-deplete rats or Ringer solution produced normal feedback responses (EPF40-0 = 15.4 +/- 2.0 and 10.6 +/- 1.7 nl/min, respectively). In salt-deplete rats, endogenous tubular fluid and Ringer solution produced feedback responses of similar magnitude (EPF40-0 = 14.2 +/- 1.8 and 13.0 +/- 2.0 nl/min, respectively) but exogenous tubular fluid from salt-loaded rats elicited only a small feedback response (EPF40-0 = 1.5 +/- 1.6 nl/min), indistinguishable from that seen in salt-loaded rats with endogenous tubular fluid. It is concluded that an inhibitory factor in the tubular fluid of chronically salt-loaded rats causes a reduction in tubuloglomerular feedback response.

Tubuloglomerular feedback and tubular reabsorption during acute potassium loading in rats

1994 ◽  
Vol 267 (2) ◽  
pp. F223-F230 ◽  
Author(s):  
B. Braam ◽  
P. Boer ◽  
H. A. Koomans
Keyword(s):  
Distal Tubule ◽  
Plasma Potassium ◽  
Tubuloglomerular Feedback ◽  
Control Group ◽  
Sprague Dawley ◽  
Time Control ◽  
Sprague Dawley Rats ◽  
Single Nephron ◽  
Flow Pressure ◽  
Potassium Loading

Acute hyperkalemia has been associated with changes in reabsorption, glomerular filtration rate (GFR), and autoregulation, which might represent altered tubuloglomerular feedback (TGF) responsiveness. Therefore, TGF responsiveness, segmental reabsorption of water, sodium and potassium, and single-nephron GFR were evaluated during acute potassium loading in male Sprague-Dawley rats. Rats receiving 300 mM KNO3, KHCO3, and KCl showed significantly increased plasma potassium levels and attenuation of stop-flow pressure responses 45-90 min after starting the potassium infusion compared with that observed in time controls and rats infused with 300 mM NaCl. Attenuation of TGF responsiveness could not be related to plasma and kidney angiotensin II levels. Segmental water and sodium handling and proximal to distal single-nephron GFR differences assessed in a time control group and a group receiving 300 mM KCl revealed no changes related to KCl infusion. However, late proximal and early distal potassium concentrations increased significantly from 4.7 +/- 0.2 to 6.3 +/- 0.3 mM (P < 0.01) and from 1.5 +/- 0.1 to 2.7 +/- 0.4 mM (P < 0.01), respectively. In summary, although attenuated TGF responsiveness was demonstrated at higher perfusion rates, this study does not support a significant role for either the TGF mechanism or changes in reabsorption upstream of the early distal tubule for the initiation of kaliuresis during acute potassium loading.

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