Antibody and complement reduce renal hemodynamic function in isolated perfused rat kidney

1996 ◽  
Vol 270 (1) ◽  
pp. F179-F185 ◽  
Author(s):  
T. Jocks ◽  
G. Zahner ◽  
U. Helmchen ◽  
U. Kneissler ◽  
R. A. Stahl
Keyword(s):  
Rat Kidney ◽  
Glomerular Injury ◽  
Hemodynamic Changes ◽  
Synthesis Inhibitor ◽  
Rat Serum ◽  
Renal Hemodynamic ◽  
Perfusate Flow ◽  
Perfused Rat Kidney ◽  
Renal Vascular

To evaluate the effect of antibody and complement on renal hemodynamic changes, glomerular injury was induced in isolated perfused kidneys by an anti-thymocyte antibody (ATS) and rat serum (RS). Glomerular filtration rate (GFR), renal vascular resistance (RVR), and renal perfusate flow (RPF) were assessed over an 80-min period. The possible role of thromboxane (Tx) was tested by the application of the Tx synthesis inhibitor UK-38485 and the Tx receptor blocker daltroban. Perfusion of kidneys with ATS and RS significantly reduced GFR at 10 min (control, 501 +/- 111; ATS + RS, 138 +/- 86 ml.g kidney-1.min-1, significance of F = 0.000) after RS. Similarly, RPF (ml.g kidney-1.min-1) fell from 19.2 +/- 1.8 to 6.1 +/- 2.0 (significance of F = 0.000), whereas RVR (mmHg.ml-1.g.min) increased threefold from 5.2 +/- 0.4 to 17.9 +/- 5.0 at 10 min. These changes were ameliorated by the pretreatment of the rats with daltroban and UK-38485. Addition of erythrocytes to the perfusate increased RVR and GFR, whereas RPF decreased compared with cell-free perfused kidneys. ATS and RS in this preparation also decrease GFR and RPF. The hemodynamic alterations appeared without changes in filtration fraction. Compared with untreated, perfused control kidneys, glomerular Tx formation was significantly increased in ATS and RS perfused kidneys. These data demonstrate that antibody and RS induce impairment of renal hemodynamics, which are mediated by increased Tx formation.

Effects of adenosine receptor antagonists on the responses to contrast media in the isolated rat kidney

2000 ◽  
Vol 98 (3) ◽  
pp. 303-311 ◽  
Author(s):  
Simon D. OLDROYD ◽  
Lu FANG ◽  
John L. HAYLOR ◽  
Michael S. YATES ◽  
A. Meguid EL NAHAS ◽  
...  
Keyword(s):  
Contrast Media ◽  
Receptor Antagonist ◽  
Mesangial Cell ◽  
Rat Kidney ◽  
Perfusate Flow ◽  
Perfused Rat Kidney ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Renal Vascular

Contrast media can induce both a decrease in renal blood flow and a reduction in glomerular filtration rate (GFR) when administered to both experimental animals and humans. In the present study we have examined the role of adenosine in mediating these effects using the isolated perfused rat kidney. Kidneys were perfused with a 6.7%-(w/v)-albumin-based perfusate supplemented with glucose and amino acids (n = 6 per group). They were exposed to diatrizoate [20 mg of iodine (mgI)/ml; osmolality 1650 mOsm/kg of water] or iotrolan (20 mgI/ml; osmolality 320 mOsm/kg of water) in the presence or absence of theophylline (10.8 µg/ml), or to diatrizoate in the presence or absence of a specific adenosine A1 receptor antagonist (KW-3902; 2 µg/ml) or a specific A2 receptor antagonist (KF17837; 6 µg/ml). Diatrizoate (n = 6) produced a fall in GFR from 0.65±0.04 to 0.42±0.03 ml·min-1·g-1 (P < 0.05); renal perfusate flow (RPF) also declined, from 36.5±3.8 to 22.0±3.2 ml·min-1·g-1 (P < 0.05). Iotrolan (n = 6) produced a fall in GFR from 0.64±0.02 to 0.48±0.04 ml·min-1·g-1 (P < 0.05) and in RPF from 33.3±3.8 to 24.0±3.0 ml·min-1·g-1 (P < 0.05). Theophylline (10.8 µg/ml) prevented the fall in GFR caused by either diatrizoate (baseline, 0.63±0.05 ml·min-1·g-1; diatrizoate+theophylline, 0.60±0.04 ml·min-1·g-1) or iotrolan (basline, 0.64±0.04 ml·min-1·g-1; iotrolan+theophylline, 0.67±0.05 ml·min-1·g-1), but did not affect the decreases in RPF caused by either agent. KW-3902 (2 µg/ml) also prevented the fall in GFR produced by diatrizoate (baseline, 0.66±0.05 ml·min-1·g-1; diatrizoate+KW-3902, 0.61±0.05 ml·min-1·g-1), while the fall in RPF remained unaffected. KF17837 (6 µg/ml) had no effect on the decreases in either GFR or RPF induced by diatrizoate (n = 6 per group). The results suggest a role for adenosine acting at the A1 receptor in mediating the decrease in GFR induced by contrast media. This effect is independent of a change in renal vascular resistance, and possibly secondary to mesangial cell contraction causing a decrease in the ultrafiltration coefficient.

Ca-dependent hemodynamic and natriuretic effects of atrial extract in isolated rat kidney

1984 ◽  
Vol 246 (4) ◽  
pp. F447-F456 ◽  
Author(s):  
M. J. Camargo ◽  
H. D. Kleinert ◽  
S. A. Atlas ◽  
J. E. Sealey ◽  
J. H. Laragh ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Fractional Excretion ◽  
Electrolyte Excretion ◽  
Renal Vasculature ◽  
Filtration Fraction ◽  
Perfused Rat Kidney ◽  
Site Of Action ◽  
Initial Control ◽  
Renal Vascular

The effects of rat atrial tissue extract on renal hemodynamics and fluid and electrolyte excretion were investigated in the isolated perfused rat kidney (IK). IK were perfused at a constant effective perfusion pressure of about 90 mmHg. After control clearance periods (C), extracts of rat atria (AE) or ventricles (VE) were added to the perfusate and three 10-min experimental periods followed. AE, but not VE, significantly increased (P less than 0.001) renal vascular resistance (RVR) to 133 +/- 8% of C, GFR to 201 +/- 34%, filtration fraction to 245 +/- 41%, urine flow (V) to 675 +/- 131%, fractional excretion (FE) of H2O to 336 +/- 29%, absolute Na excretion (UNaV) to 1,259 +/- 290%, FENa to 642 +/- 129%, UKV to 2,226 +/- 1,237%, and FEK to 542 +/- 119%. Despite the marked natriuresis, since GFR doubled, Na reabsorption rose from 78.3 +/- 36.3 in C to 132 +/- 36.3 mueq/min after AE. The effects of AE were immediate and lasted to the end of the perfusion. The lower the initial control GFR, the larger was the AE-induced increase in GFR. Perfusion with low [Ca] (0.2 mM) or verapamil (10(-5) M) severely blunted the hemodynamic, diuretic, kaliuretic, and natriuretic effects of AE. AE decreased rather than increased the RVR when IK were perfused with vasoconstrictors such as angiotensin II, norepinephrine, or vasopressin. The results demonstrate that AE acts directly on the kidney, eliciting powerful Ca-dependent hemodynamic and natriuretic responses. The natriuresis induced by AE can be accounted for, at least in part, by its renal hemodynamic effects rather than by the presence of a putative tubular natriuretic factor. The hypothesis is advanced that AE contains a substance(s) which behaves as a functional agonist/antagonist of endogenous vasoconstrictors with a preferential site of action on the efferent arterioles of the renal vasculature.

Nitric oxide enhancement of erythropoietin production in the isolated perfused rat kidney

1995 ◽  
Vol 269 (4) ◽  
pp. C917-C922 ◽  
Author(s):  
K. Yoshioka ◽  
J. W. Fisher
Keyword(s):  
Nitric Oxide ◽  
Rat Kidney ◽  
Mrna Levels ◽  
Isolated Perfused Rat Kidney ◽  
Intracellular Cgmp ◽  
Perfused Rat Kidney ◽  
Arterial Po2

We have previously reported that nitric oxide (NO) and guanosine 3',5'-cyclic monophosphate (cGMP) may be involved in the regulation of erythropoietin (Epo) production in response to hypoxia both in vivo and in vitro (20). In the present studies, we have used the isolated perfused rat kidney to assess the role of NO in oxygen sensing and Epo production. When arterial PO2 was reduced from 100 mmHg (normoxemic) to 30 mmHg (hypoxemic) in the perfusate of this system, perfusate levels of Epo were significantly increased. This hypoxia-induced increase in Epo production was significantly decreased by the addition of NG-nitro-L-arginine methyl ester (L-NAME; 1 mM) to the perfusates. Hypoxemic perfusion also produced a significant increase, and L-NAME significantly inhibited this increase, in intracellular cGMP levels in the kidney when compared with normoxemic perfused kidneys. Quantitative reverse transcription-polymerase chain reaction also revealed that hypoxemic perfusion produced significant increases in Epo mRNA levels in the kidney, which was blocked by L-NAME. Our findings further support an important role for the NO/cGMP system in hypoxic regulation of Epo production.

The Effects of Calcium and Calcium-Ionophores (X 537 a and a 23187) on Renin Release in the Isolated Perfused Rat Kidney

1978 ◽  
Vol 55 (s4) ◽  
pp. 163s-166s ◽  
Author(s):  
U. Schwertschlag ◽  
E. Hackenthal ◽  
R. Hackenthal ◽  
G. H. Rohs
Keyword(s):  
Indirect Effect ◽  
Indirect Effects ◽  
Vascular Tone ◽  
Rat Kidney ◽  
Renin Release ◽  
Direct And Indirect Effects ◽  
Calcium Depletion ◽  
A 23187 ◽  
Perfusate Flow ◽  
Perfused Rat Kidney

1. Calcium depletion from the medium of the isolated perfused kidney reduced renin release and renal perfusate flow. 2. Reintroduction of calcium increased renin release and perfusate flow. 3. The ionophore X 537 A (0·1–4 μmol/l) increased renin release both in the presence and absence of calcium in the medium. 4. The ionophore A 23187 (1–10 nmol/l) increased as well as decreased renin release. There was a positive correlation between direction of this effect and renal perfusate flow. 5. The results are compatible with the view that the effects of calcium and ionophores on renin release are the sum of direct and indirect effects of these agents, the predominant indirect effect being the modification of vascular tone.

Renal vascular responses of kinins in the isolated perfused rat kidney

1997 ◽  
Vol 15 (11) ◽  
pp. 1349
Author(s):  
K Bagate ◽  
L Dévélioglu ◽  
B Michel ◽  
M Grima ◽  
J-L Imbs ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Vascular Responses ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Renal Vascular

Selective decrement of anionic immunoglobulin clearance after induced renal hemodynamic changes in diabetic patients

1992 ◽  
Vol 262 (3) ◽  
pp. F381-F388
Author(s):  
U. Di Mario ◽  
S. Bacci ◽  
S. Morano ◽  
G. Pugliese ◽  
P. Pietravalle ◽  
...  
Keyword(s):  
Intravenous Injection ◽  
Enzyme Inhibitor ◽  
Renal Plasma Flow ◽  
Diabetic Patients ◽  
Type I ◽  
Hemodynamic Changes ◽  
Provocative Test ◽  
Renal Hemodynamic ◽  
Renal Vascular ◽  
Group 1

The charge permselectivity of proteins was evaluated in diabetic patients after systemic and renal hemodynamic changes induced by an intravenous injection of an angiotensin-converting enzyme inhibitor (captopril) or of clonidine. Anionic immunoglobulin clearance (IgG4) was compared with that of total immunoglobulins, which have the same size but are mostly cationic, and of albumin. Ten type I hypertensive diabetic patients (group 1), 10 type 2 hypertensive diabetic patients (group 2), 5 type 1 normotensive diabetic patients (group 3), 10 subjects with essential hypertension (group 4), and 7 normal volunteers (group 5) received an intravenous injection of captopril (25 mg/100 ml in 5 min). Twelve of the hypertensive diabetic patients underwent a second provocative test with clonidine (150 micrograms/100 ml) (group 6) or placebo (100 ml saline) (group 7) with the same procedure. None of the patients had clinical nephropathy or other disorders. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured before and during the tests. A significant decrease in diastolic blood pressure was observed in groups 1, 2, 4, and 6, together with an increase in the GFR and RPF values in groups 1, 2, 3, and 4 only, as well as a decrease in renal vascular resistances in groups 1, 2, 3, 4, and 6. Both clearances and fractional clearances of IgG4 and IgG decreased after captopril in groups 1 and 2.2+ The decrease in IgG4 clearance was correlated to that of renal vascular resistances in group 1 patients. A significant decrease in the anionic-cationic immunoglobulin ratio (IgG4/IgG) was observed in groups 1, 2, and 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of neuronal nitric oxide synthase in mediating renal hemodynamic changes during pregnancy

2001 ◽  
Vol 281 (5) ◽  
pp. R1390-R1393 ◽  
Author(s):  
S. R. Abram ◽  
B. T. Alexander ◽  
W. A. Bennett ◽  
J. P. Granger
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Renal Plasma Flow ◽  
Neuronal Nitric Oxide Synthase ◽  
Hemodynamic Changes ◽  
Pregnant Rats ◽  
Renal Hemodynamic ◽  
Oxide Synthase ◽  
Nnos Inhibition

Renal plasma flow (RPF) and glomerular filtration rate (GFR) are markedly increased during pregnancy. We recently reported that the renal hemodynamic changes observed during pregnancy in rats are associated with enhanced renal protein expression of neuronal nitric oxide synthase (nNOS). The purpose of this study was to determine the role of nNOS in mediating renal hemodynamic changes observed during pregnancy. To achieve this goal, we examined the effects of the nNOS inhibitor 7-nitroindazole (7-NI) on kidney function in normal conscious, chronically instrumented virgin ( n = 6) and pregnant rats ( n = 9) at day 16 of gestation. Infusion of 7-NI had no effect on RPF (4.7 ± 0.7 vs. 4.8 ± 0.9 ml/min), GFR (2.2 ± 0.2 vs. 2.5 ± 0.4 ml/min), or mean arterial pressure (MAP; 127 ± 7 vs. 129 ± 10 mmHg) in virgin rats. In contrast, 7-NI infused into pregnant rats decreased RPF (8.9 ± 1.6 vs. 6.5 ± 1.4 ml/min) and GFR (4.4 ± 0.7 vs. 3.3 ± 0.7 ml/min) while having no effect on MAP (123 ± 4 vs. 123 ± 3 mmHg). In summary, inhibition of nNOS in pregnant rats at midgestation results in significant decreases in RPF and GFR. nNOS inhibition in virgin rats had no effect on renal hemodynamics. These data suggest that nNOS may play a role in mediating the renal hemodynamic changes that occur during pregnancy.

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