Inter-Relationship between Autoregulation of Glomerular Filtration Rate, Tubuloglomerular Feedback and Juxtaglomerular Renin Activity in Normotensive and Hypertensive Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 105s-107s
Author(s):  
J. Schnermann ◽  
D. W. Ploth ◽  
H. Dahlheim
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renin Angiotensin System ◽  
Feedback Regulation ◽  
Renal Perfusion ◽  
Tubuloglomerular Feedback ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Proximal Tubular

1. Reduction of renal perfusion pressure from 133 mmHg to 117 mmHg in control rats did not induce a significant change of kidney glomerular filtration rate (GFR) or nephron GFR determined in distal tubules. In contrast, nephron GFR measured in proximal tubular segments (NGFR-P) fell significantly. 2. Qualitatively the same response of filtration rate to changes of arterial blood pressure was found in the chronically clipped kidneys of Goldblatt hypertensive rats after acute removal of the clip. 3. In contrast, autoregulation of kidney GFR, NGFR-D and NGFR-P was abolished in the contralateral kidneys of Goldblatt hypertensive rats. 4. Microperfusion studies showed that tubuloglomerular feedback regulation of NGFR was present in the renin-rich ischaemic kidneys of Goldblatt rats after removal of the constricting clip, but greatly attenuated in the renin-depleted contralateral kidneys. 5. These data indicate that tubuloglomerular feedback participates in establishing renal autoregulation, possibly by mediation of the renin-angiotensin system.

Increased tubuloglomerular feedback activity in Milan hypertensive rats

1986 ◽  
Vol 250 (6) ◽  
pp. F967-F974 ◽  
Author(s):  
U. Boberg ◽  
A. E. Persson
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Tubuloglomerular Feedback ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Single Nephron ◽  
Flow Pressure ◽  
Normotensive Strain

Studies of whole-kidney function and micropuncture measurements in superficial nephrons were performed to investigate the role of the tubuloglomerular feedback (TGF) in the excretion of salt and water in hydropenic and volume-expanded rats of the spontaneously hypertensive Milan strain (MHS). The rats were 3.5-5 and 5-7 wk old, and age-matched animals from the Milan normotensive strain (MNS) served as controls. There was no difference in mean arterial blood pressure (Pa) between the 3.5- to 5-wk-old prehypertensive MHS (MHSp) and MNS rats, but the glomerular filtration rate (GFR) was higher in MHSp than in MNS [1.35 vs. 0.80 ml X min-1 X g kidney wt (KW)-1, P less than 0.01]. The distal single-nephron glomerular filtration rate (SNGFR) was also higher in MHSp than in MNS (28.6 vs. 20.2 nl X min-1 X g KW-1, P less than 0.05). TGF was determined from both stop-flow pressure response and proximal and distal SNGFR. It was found that MHSp exhibited essentially no TGF response. During development of hypertension 5- to 7-wk-old MHS (MHSd) had a higher Pa than MNS (120 vs. 98 mmHg, P less than 0.01). Normally GFR and SNGFR increase with age, and such was the case with MNS (0.8 to 1.02 ml X min-1 X g KW-1 and 20.2 to 23.4 nl X min-1 X g KW-1), but in MHSd there was a decrease in both GFR and SNGFR with age (1.35 to 1.10 ml X min-1 X g KW-1 and 28.3 to 18.3 nl X min-1 X g KW-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Feedback mediation of SNGFR autoregulation in hydropenic and DOCA- and salt-loaded rats

1979 ◽  
Vol 237 (1) ◽  
pp. F63-F74 ◽  
Author(s):  
L. C. Moore ◽  
J. Schnermann ◽  
S. Yarimizu
Keyword(s):  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Tubuloglomerular Feedback ◽  
Single Nephron ◽  
Proximal Tubular

Tubuloglomerular feedback (TGF) mediation of autoregulation was investigated by measuring the response of single nephron glomerular filtration rate (SNGFR) to changes in arterial pressure (AP) following acute or chronic TGF inhibition. In hydropenic rats with intact TGF, distal SNGFR was 25.0 +/- 1.2 (SE) and 23.9 +/- 1.4 nl/min at AP of 111 and 135 mmHg, respectively. In the same 20 nephrons during proximal tubular microinfusion of furosemide, distal SNGFR was 23.6 +/- 1.4 (n = 16) and 29.7 +/- 1.4 nl/min (n = 20) (P less than 0.001, n = 16) at 112 and 133 mmHg. When determined proximally, SNGFR was 25.6 +/- 1.0 and 29.5 +/- 0.9 nl/min (P less than 0.001, n = 31) at 112 and 157 mmHg; kidney GFR increased similarly. These data and the predictions of a GFR model were then used to estimate autoregulatory efficiency. This analysis indicated that partial autoregulation occurred during TGF inhibition. Therefore, TGF is an essential, but probably not the only, mechanism mediating SNGFR autoregulation.

The Effect of Glucagon on Glomerular Filtration Rate in Dogs During Reduction of Renal Blood Flow

1975 ◽  
Vol 53 (4) ◽  
pp. 660-668 ◽  
Author(s):  
Mortimer Levy
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Acute Tubular Necrosis ◽  
Filtration Rate ◽  
Renal Perfusion ◽  
Beneficial Effects ◽  
Tubular Necrosis ◽  
Arterial Blood ◽  
Urine Formation

Glucagon in small intravenous (i.v.) doses markedly increases glomerular filtration rate (GFR) in normal anesthetized dogs. In this study, the effects of glucagon 5 μg/min (i.v.) on renal hemodynamics was tested in four canine models of acute pre-renal failure (hemorrhage, barbiturate overdose; renal arterial clamping and renal arterial infusions of noradrenaline) and in a model of unilateral acute tubular necrosis at 4 h and 6–7 days following completion of the ischemic insult. Following hemorrhage and barbiturate excess, with arterial blood pressure maintained at 65–70 mm Hg, whole-kidney GFR and clearance rate of p-aminohippurate decreased by 50–70%. During this reduction of perfusion pressure, the subsequent infusion of glucagon increased GFR by 90–130%. In models where arterial pressure was normal during the period of ischemia (clamping and noradrenaline infusion), not only did glucagon significantly increase renal perfusion, but the ischemic kidney proved to be far more sensitive to the hemodynamic effects of glucagon (ΔGFR = 120–160%) than the contralateral control (ΔGFR = 30–40%). In three dogs completely anuric following renal arterial clamping, glucagon was able to improve blood flow and restart urine formation. Glucagon, but not dopamine, was able to simulate the beneficial effects of hypertonic mannitol on renal function in dogs with hemorrhagic hypotension. Glucagon was without effect in established acute tubular necrosis. This study, therefore, indicates that, during renal ischemia, glucagon may be quite effective in preserving urine output and perfusion of the kidneys.

Abolished tubuloglomerular feedback and increased plasma renin in adenosine A1 receptor-deficient mice

2001 ◽  
Vol 281 (5) ◽  
pp. R1362-R1367 ◽  
Author(s):  
Russell Brown ◽  
Anna Ollerstam ◽  
Björn Johansson ◽  
Ole Skøtt ◽  
Samuel Gebre-Medhin ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Knockout Mice ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Tubuloglomerular Feedback ◽  
Wild Type ◽  
Proximal Tubular ◽  
A1 Receptor ◽  
Tubular Flow

The hypothesis that adenosine acting on adenosine A1 receptors (A1R) regulates several renal functions and mediates tubuloglomerular feedback (TGF) was examined using A1R knockout mice. We anesthetized knockout, wild-type, and heterozygous mice and measured glomerular filtration rate, TGF response using the stop-flow pressure (Psf) technique, and plasma renin concentration. The A1R knockout mice had an increased blood pressure compared with wild-type and heterozygote mice. Glomerular filtration rate was similar in all genotypes. Proximal tubular Psf was decreased from 36.7 ± 1.2 to 25.3 ± 1.6 mmHg in the A1R+/+ mice and from 38.1 ± 1.0 to 27.4 ± 1.1 mmHg in A1R+/− mice in response to an increase in tubular flow rate from 0 to 35 nl/min. This response was abolished in the homozygous A1R−/− mice (from 39.1 ± 4.1 to 39.2 ± 4.5 mmHg). Plasma renin activity was significantly greater in the A1R knockout mice [74.2 ± 14.3 milli-Goldblatt units (mGU)/ml] mice compared with the wild-type and A1R+/− mice (36.3 ± 8.5 and 34.1 ± 9.6 mGU/ml), respectively. The results demonstrate that adenosine acting on A1R is required for TGF and modulates renin release.

Dynamics of intrarenal pressures and glomerular filtration rate after acetazolamide

1991 ◽  
Vol 261 (1) ◽  
pp. F169-F178 ◽  
Author(s):  
P. P. Leyssac ◽  
F. M. Karlsen ◽  
O. Skott
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Feedback Mechanism ◽  
Tubuloglomerular Feedback ◽  
Proximal Tubular ◽  
51Cr Edta ◽  
Level 3 ◽  
Reabsorption Rate ◽  
Fluid Conductivity

The dynamics of intrarenal pressures, early distal tubular fluid conductivity (EDC), and renal flood flow (RBF) were studied in rats given acetazolamide (ACZ), an inhibitor of proximal reabsorption. Glomerular filtration rate (GFR) and end-proximal flow were estimated by clearances of 51Cr-EDTA and lithium. Proximal tubular pressure (Pprox) increased initially by 1.7 +/- 0.1 mmHg after ACZ, causing a decrease in the hydrostatic pressure difference across the glomerular membrane (delta P). EDC increased, and then RBF, glomerular capillary pressure (Pgc), Pprox, and star vessel pressures (Psv) dropped as a result of afferent vasoconstriction. Pprox decreased less than Pgc, resulting in a further decrease in delta P, which after 25–30 s reached a constant level 3-4 mmHg below control. After a transient increase the pressures declined to a new steady state, in which Pprox was equal to control, Pgc was decreased, and distal tubular pressure, end-proximal flow, and EDC were increased. GFR was depressed by 29%. The results indicate that the tubuloglomerular feedback mechanism controls Pgc and Pprox by afferent vasoconstriction, as well as efferent vasodilation. The data also indicate that proximal reabsorption rate is important in determining the changes in delta P by its effect on Pprox at least in the early transient phase.

Angiotensin-mediated alterations in nephron function in Goldblatt hypertensive rats

1982 ◽  
Vol 243 (6) ◽  
pp. F553-F560 ◽  
Author(s):  
W. C. Huang ◽  
D. W. Ploth ◽  
L. G. Navar
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Enzyme Inhibitor ◽  
Distal Tubule ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Nephron Segment ◽  
Single Nephron

The present study was performed to evaluate superficial nephron responses of the nonclipped kidney to angiotensin I converting enzyme inhibitor (CEI) (SQ 20,881, 3 mg . kg-1 . h-1) in two-kidney, one-clip Goldblatt hypertensive (GH) rats. Late proximal and early distal tubule collections were obtained before and during CEI. Significant increases in glomerular filtration rate, urine flow, sodium excretion, proximal and distal tubule flow rates, and single nephron glomerular filtration rate (from 24.6 +/- 1.7 to 27.5 +/- 1.6 nl/min) occurred despite reductions in arterial blood pressure (from 160 +/- 5 to 137 +/- 6 mmHg) during CEI. Proximal tubule absolute and fractional reabsorption of fluid, chloride, and total solute decreased significantly. In the nephron segment between the two collection sites, there were increases in absolute but decreases in fractional reabsorption. At the distal tubule level, fractional reabsorption but not absolute reabsorption decreased significantly. Proximal and distal tubule hydrostatic pressures increased significantly while peritubular capillary pressure decreased slightly. Responses following inhibition of angiotensin II formation suggest that there exists an angiotensin II-mediated enhancement in tubular reabsorption in the nonclipped kidney of Goldblatt hypertensive rats.

On determinants of glomerular filtration rate after inhibition of proximal tubular reabsorption

1994 ◽  
Vol 266 (5) ◽  
pp. R1544-R1550 ◽  
Author(s):  
P. P. Leyssac ◽  
F. M. Karlsen ◽  
N. H. Holstein-Rathlou ◽  
O. Skott
Keyword(s):  
Glomerular Filtration Rate ◽  
Carbonic Anhydrase ◽  
Glomerular Filtration ◽  
Flow Resistance ◽  
Filtration Rate ◽  
Tubuloglomerular Feedback ◽  
Parallel Change ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Distal Flow

The carbonic anhydrase inhibitor acetazolamide (ACZ) inhibits the absolute rate of proximal reabsorption (APR), causes a reduction in glomerular filtration rate (GFR), and activates the tubuloglomerular feedback mechanism (TGF) resulting in afferent vasoconstriction. The quantitative importance of the afferent vasoconstriction for the reduced GFR was tested by addition of a vasodilator during continuous infusion of ACZ. Dopamine caused an increase in renal blood flow (RBF) to pre-ACZ levels. Glomerular capillary pressure (Pgc) and proximal tubular pressure (Pprox) increased in parallel (by 3.1 and 3.0 mmHg, respectively) leaving pressure gradient (delta P) unchanged. APR, as estimated from the clearances of 51Cr-EDTA and lithium, remained unchanged. Urine flow almost doubled. GFR was only modestly reversed (pre-ACZ/ACZ/ACZ+dopamine: 100/77/83%). It is concluded that relieving the afferent vasoconstriction seen after carbonic anhydrase inhibition fails to restore GFR to its control value. This is due to the high flow resistance in the distal nephron segments during the increased tubular flow rates seen after ACZ. The high distal flow resistance causes a parallel change in Pgc and Pprox and thus leaves delta P nearly unchanged. The present study highlights the importance of the distal flow resistance in determining delta P and therefore GFR during conditions where tubular flow rate is increased.

Effects of simultaneous infusions of glucagon and cyclic AMP on glomerular filtration rate in the dog

1978 ◽  
Vol 56 (4) ◽  
pp. 596-602 ◽  
Author(s):  
Enrique Espinosa-Meléndez ◽  
Mortimer Levy
Keyword(s):  
Glomerular Filtration Rate ◽  
Cyclic Amp ◽  
Renal Artery ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Perfusion ◽  
Left Renal Artery ◽  
Arterial Blood ◽  
Intracellular Release ◽  
The Right

In this study, we tested the hypothesis that the renal vasodilator properties of glucagon are mediated by the intracellular release of cyclic AMP. In eight normal dogs, we tested the effect on glomerular filtration rate (GFR) of intravenous glucagon (5 μg/min), after having administered cyclic AMP (1.6 mg/min) into the left renal artery. GFR for both the right and left kidneys increased by 38% (p < 0.05), compared with an increment of 29% when glucagon alone had previously been administered. Similar studies were carried out in five dogs with steady-state hemorrhagic hypotension (arterial blood pressure = 75 mmHg). In this group as well, the prior infusion of cyclic AMP did not blunt or abolish the tendency of glucagon to promote renal perfusion or increase GFR. When cyclic AMP was administered alone, GFR and the clearance of p-aminohippurate usually declined by about 20% (p < 0.05). In six dogs, glucagon was administered intravenously at 5 μg/min prior to the infusion of cyclic AMP (1.6 mg/min) into the left renal artery. For this kidney, the anticipated decline in renal perfusion occurred. The prior administration of theophylline into the left renal artery did not prevent an intravenous infusion of glucagon from elevating GFR. These experiments indicate that the prior flooding of the microvasculature with either cyclic AMP or glucagon does not prevent the pharmacological effects of each of these substances. The renal hemodynamic effects of glucagon in normal and hypotensive dogs does not appear to depend on the release of cyclic AMP.

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