scholarly journals Effects of thromboxane A2 receptor blockade on oliguric ischemic acute renal failure in conscious rats.

1993 ◽  
Vol 4 (1) ◽  
pp. 50-57
Author(s):  
H J Kramer ◽  
M G Mohaupt ◽  
F Pinoli ◽  
A Bäcker ◽  
H Meyer-Lehnert ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Urine Volume ◽  
Atp Synthesis ◽  
Thromboxane A2 ◽  
Left Renal Artery ◽  
Receptor Blockade ◽  
Sprague Dawley ◽  
Ischemic Acute Renal Failure

To investigate the potential pathogenetic and therapeutic roles of thromboxane A2 (TXA2) and its receptor blockade, respectively, in the early phase of ischemic acute renal failure (ARF), renal function, TXB2 excretion, and the effects of the specific TXA2 receptor antagonist sulotroban (SU) in a model of unilateral renal artery occlusion in conscious female Sprague-Dawley rats were studied. Occlusion of the left renal artery for 1 h in untreated (i.e., vehicle-treated) rats (N = 8) resulted in oliguric ARF. In SU-treated rats (N = 8), the drug was given as an i.v. bolus of 5 mg/kg body wt, followed by a continuous infusion of 0.5 mg/min.kg body wt from 1 h before and during ischemia and for 6 h after reflow. After 1 h of ischemia, urine volume of left ischemic kidneys from untreated rats had decreased from 13.2 +/- 2.8 to 1.0 +/- 0.3 and 0.5 +/- 0.2 microL/min.100 g at 2 and 6 h of reflow, respectively, and GFR had decreased from 0.32 +/- 0.04 mL/min.100 g body wt to undetectable values. At 6 h of reflow, medullary Na-K-ATPase was slightly (P < 0.05) reduced in left ischemic kidneys, whereas medullary and papillary enzyme activities were compensatorily increased (P < 0.01) in right intact kidneys. The ADP/O ratio of cortical mitochondria was 41% (P < 0.05) and ATP synthesis was 77% (P < 0.01) lower than in right intact kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

Glomerular endothelin receptors during initiation and maintenance of ischemic acute renal failure in rats

1991 ◽  
Vol 260 (1) ◽  
pp. F110-F118
Author(s):  
B. M. Wilkes ◽  
A. R. Pearl ◽  
P. F. Mento ◽  
M. E. Maita ◽  
C. M. Macica ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Acid Treatment ◽  
Affinity Constant ◽  
Left Renal Artery ◽  
Sprague Dawley ◽  
Receptor Sites ◽  
Sprague Dawley Rats ◽  
Receptor Number ◽  
Ischemic Acute Renal Failure

Glomerular endothelin (ET) receptors were studied in normal Sprague-Dawley rats and in rats with ischemic acute renal failure (ARF) induced by a 60-min occlusion of the left renal artery (right kidney intact). In normal rats ET bound to specific glomerular receptor sites [equilibrium affinity constant (Kd), 46.6 +/- 5.8 pM; receptor number (Ro), 1,167 +/- 160 fmol/mg (n = 7)]. ET infusion (90 ng.kg-1.min-1, intra-arterially) raised mean arterial pressure by 32 +/- 4 mmHg, lowered renal blood flow (RBF) by 62% and glomerular filtration rate (GFR) by 49%, and reduced the number of glomerular ET receptor sites by 62%. Reduced ET binding could not be explained by prior occupancy, because acid treatment (which dissociates bound ET from its receptors) did not increase receptor number. If elevated ET levels contributed to decreased RBF and GFR in ARF, glomerular ET receptors would be expected to down-regulate. In rats with ischemic ARF there were no differences in the number or affinity of glomerular ET receptors in the clamped or contralateral kidneys. Additional studies demonstrated that the downregulation response to ET infusion was intact in ARF. The data demonstrate that glomerular ET receptors are unaltered in ischemic ARF and do not support a role for increased glomerular ET in the alterations of renal hemodynamics in this model.

Role of CD11a and CD11b in ischemic acute renal failure in rats

1994 ◽  
Vol 267 (6) ◽  
pp. F1052-F1058 ◽  
Author(s):  
H. Rabb ◽  
C. C. Mendiola ◽  
J. Dietz ◽  
S. R. Saba ◽  
T. B. Issekutz ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Complete Blood Count ◽  
Leukocyte Adhesion ◽  
Treated Group ◽  
Organ Injury ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Ischemic Acute Renal Failure

Leukocytes, particularly neutrophils, have been implicated in ischemic-reperfusion organ injury (IRI). However, their role in kidney IRI is controversial. Leukocytes express the adhesion molecules CD11/CD18 on their surface, which mediate many functions that can lead to tissue damage. To determine the role of CD11a and CD11b in IRI in the kidney, uninephrectomized Sprague-Dawley rats were pretreated with monoclonal antibodies (MAbs) directed against CD11a and CD11b or control MAbs. The serum creatinine (SCr), complete blood count, and kidney histopathological damage scores (PDS) (scale: 0-4) were assessed prior to and 24 h after 60 min of ischemia. Mean SCr 24 h after ischemia was significantly decreased in the anti-CD11a- and -CD11b-treated group compared with the control MAb-treated group (2.5 +/- 0.3 mg/dl vs. 3.4 +/- 0.2 mg/dl, P <0.05). PDS were also reduced in the CD11a and CD11b group compared with controls (2.7 +/- 0.2 vs. 3.5 +/- 0.1, P < 0.001). These data show that the CD11/CD18 leukocyte adhesion pathway plays a role in mediating ischemic acute renal failure in rats.

Effect of renal ischemia on cortical microsomal calcium accumulation

1985 ◽  
Vol 249 (5) ◽  
pp. C476-C483 ◽  
Author(s):  
A. Schieppati ◽  
P. D. Wilson ◽  
T. J. Burke ◽  
R. W. Schrier
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Normal Level ◽  
Mitochondrial Respiration ◽  
Renal Cortex ◽  
Bilateral Renal Artery ◽  
Ischemic Acute Renal Failure

Mitochondrial respiration, Ca2+ content, and Ca2+ kinetics have been found to be profoundly altered in ischemic acute renal failure (ARF). The effect of clamping the bilateral renal artery for 50 and 90 min on microsomal Ca2+ uptake was therefore examined in the rat. The 50-min clamping produced a reversible model of nonoliguric ARF, and the 90-min clamping produced a model of nonreversible oliguric ARF. In the 50-min nonoliguric model, ATP-dependent Ca2+ uptake by microsomes from renal cortex (nmol X mg protein-1 X 30 min-1) was significantly impaired immediately before release of the clamp and before return of renal blood flow (reflow) (191 +/- 11 vs. 83 +/- 11, P less than 0.005). However, in this nonoliguric model of ischemic ARF, microsomal uptake returned completely to normal after 1 h of reflow (sham 189 +/- 11 vs. 167 +/- 14 at 1 h, NS) and persisted at this normal level at 24 h (sham 166 +/- 14 vs. 150 +/- 13 at 24 h, NS). In the oliguric model of ARF the microsomal Ca2+ uptake also was impaired immediately after the clamp release (sham 191 +/- 11 vs. 93 +/- 11, P less than 0.001) as well as after 1 h of reflow (sham 189 +/- 11 vs. 129 +/- 12, P less than 0.005) but not at 24 h (sham 166 +/- 14 vs. 173 +/- 13, NS). The results indicate that impaired microsomal Ca2+ uptake occurs early in both oliguric and nonoliguric ARF and persists after 1 h of reflow in the oliguric model.(ABSTRACT TRUNCATED AT 250 WORDS)

Complete Resolution of Acute Renal Failure after Left Renal Artery Angioplasty and Stent Placement for Total Renal Artery Occlusion

Cardiology ◽  
2006 ◽  
Vol 108 (1) ◽  
pp. 51-54 ◽  
Author(s):  
Arshad Rehan ◽  
Yassar Almanaseer ◽  
Devang M. Desai ◽  
Arshad Ali ◽  
Hiroshi Yamasaki
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Stent Placement ◽  
Complete Resolution ◽  
Artery Occlusion ◽  
Left Renal Artery ◽  
Renal Artery Occlusion

bFGF induces an earlier expression of nephrogenic proteins after ischemic acute renal failure

2006 ◽  
Vol 291 (6) ◽  
pp. R1677-R1687 ◽  
Author(s):  
Sandra Villanueva ◽  
Carlos Cespedes ◽  
Alexis Gonzalez ◽  
Carlos P. Vio
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Damage ◽  
Kidney Development ◽  
Smooth Muscle Actin ◽  
Ischemia Reperfusion ◽  
Regeneration Process ◽  
Sprague Dawley ◽  
Wide Range ◽  
Ischemic Acute Renal Failure

Recovery from acute renal failure (ARF) requires the replacement of injured cells with new cells that restore tubule epithelial integrity. We described recently the expression of a wide range of nephrogenic proteins in tubular cells after ARF induced by ischemia-reperfusion (I/R) (Villanueva S, Cespedes C, and Vio CP. Am J Physiol Regul Integr Comp Physiol 290: R861–R870, 2006). These markers, namely, Vimentin, neural cell adhesion molecules (Ncam), basic fibroblast growth factor (bFGF), paired homeobox-2 (Pax-2), bone morphogene protein-7 (BMP-7), Noggin, Lim-1, Engrailed, Smad, phospho-Smad, hypoxia-induced factor-1α (HIF-1α), VEGF, and Tie-2, are expressed in a time frame similar to that observed in normal kidney development. bFGF participates in early kidney development as a morphogen involved in mesenchyme/epithelial transition, and it is reexpressed in the recovery phase of ARF. To test the hypothesis that bFGF can accelerate the regeneration after renal damage, we used recombinant bFGF and studied the expression pattern of the above described morphogens in ARF. Male Sprague-Dawley rats were subjected to 30 min of renal ischemic injury and were injected with bFGF 30 μg/kg followed by reperfusion. Rats were killed and the expression of nephrogenic proteins were analyzed by immunohistochemistry and Western blot analysis. In the animals subjected to I/R treated with bFGF, we observed a 12- to 24-h earlier and more abundant reexpression of the proteins Ncam, bFGF, Pax-2, BMP-7, Noggin, Lim-1, Engrailed, VEGF, and Tie-2 than the I/R untreated rats. In addition, we observed a reduction in renal damage markers ED-1 and α-smooth muscle actin. These results indicate that bFGF can participate in the regeneration process and suggest that the treatment with bFGF can induce an earlier regeneration process after ischemic acute renal failure.

scholarly journals Amelioration of ischemic acute renal failure by dietary fish oil administration in conscious dogs.

1992 ◽  
Vol 3 (6) ◽  
pp. 1312-1320
Author(s):  
H H Neumayer ◽  
M Heinrich ◽  
M Schmissas ◽  
H Haller ◽  
K Wagner ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Fish Oil ◽  
Urine Volume ◽  
Cytosolic Calcium ◽  
Unilateral Nephrectomy ◽  
Dietary Fish ◽  
Ischemic Acute Renal Failure

The hypothesis that dietary fish oil would protect dogs from ischemic acute renal failure was tested. Fish oil (eicosapentaenoic acid, 55 mg/kg per day, and docosahexaenoic acid, 40 mg/kg per day was given to eight instrumented, female, beagle dogs for 6 wk, while seven control dogs received vehicle. After 3 wk, unilateral nephrectomy was performed and a pneumatic cuff with flow probe was placed around the remaining renal artery of each dog. Three weeks thereafter, the cuff was inflated for 120 min. Renal function, RBF, and prostanoid excretion were measured 24 and 72 h after ischemia. In dogs receiving fish oil, blood pressure, GFR, RBF, renal vascular resistance (RVR), cholesterol, triglycerides, and prostanoid excretion were measured weekly for 6 wk. Further, cytosolic calcium was measured before and five times after fish oil. Blood pressure decreased, serum cholesterol and triglycerides decreased, and the cytosolic calcium within platelets decreased. The urinary excretion (expressed as picograms per milligram of creatinine) of the thromboxane (TX) metabolite TXB2 and the excretion of prostaglandin (PG)E2, as well as the excretion of the PGI2 metabolite 6-keto PGF1 alpha were decreased. GFR, RBF (Cl inulin and Cl para-aminohippuric acid), and RVR were not influenced by fish oil. Unilateral nephrectomy decreased GFR and RBF and increased RVR as expected, whereas it further decreased prostanoid excretion. Acute renal ischemia caused a significant, reversible decrease in GFR and urine volume in vehicle-treated animals, whereas no significant effect on renal function or urine volume was observed in animals pretreated with fish oil.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Simultaneous blockade of endothelin A and B receptors in ischemic acute renal failure is detrimental to long-term kidney function

2001 ◽  
Vol 59 (4) ◽  
pp. 1333-1341 ◽  
Author(s):  
Josephine Maree Forbes ◽  
Timothy David Hewitson ◽  
Gavin James Becker ◽  
Colin Lindsay Jones
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Kidney Function ◽  
Endothelin A ◽  
Ischemic Acute Renal Failure

Acute Renal Failure Due to Acute Bilateral Renal Artery Thrombosis: Successful Surgical Revascularization after Prolonged Anuria

Nephron ◽  
1990 ◽  
Vol 56 (3) ◽  
pp. 322-324 ◽  
Author(s):  
R. Pontremoli ◽  
V. Rampoldi ◽  
A. Morbidelli ◽  
F. Fiorini ◽  
A. Ranise ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Surgical Revascularization ◽  
Renal Artery Thrombosis ◽  
Artery Thrombosis ◽  
Bilateral Renal Artery

Oestrogen protects against ischaemic acute renal failure in rats by suppressing renal endothelin-1 overproduction

2002 ◽  
Vol 103 (s2002) ◽  
pp. 434S-437S ◽  
Author(s):  
Masanori TAKAOKA ◽  
Mikihiro YUBA ◽  
Toshihide FUJII ◽  
Mamoru OHKITA ◽  
Yasuo MATSUMURA
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Renal Dysfunction ◽  
Tissue Injury ◽  
Male Rats ◽  
Left Renal Artery ◽  
Protective Effects ◽  
Endothelin 1 ◽  
Ischaemia Reperfusion

We investigated whether the treatment with 17β-oestradiol has renal protective effects in male rats with ischaemic acute renal failure (ARF). We also examined if the effect of 17β-oestradiol is accompanied by suppression of enhanced endothelin-1 production in postischaemic kidneys. Ischaemic ARF was induced by clamping the left renal artery and vein for 45min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function parameters such as blood urea nitrogen, plasma creatinine and creatinine clearance were measured to test the effectiveness of the steroid hormone. Renal function in ARF rats markedly decreased 24h after reperfusion. The ischaemia/reperfusion-induced renal dysfunction was dose-dependently improved by pretreatment with 17β-oestradiol (20 or 100µg/kg, intravenously). Histopathological examination of the kidney of untreated ARF rats revealed severe lesions, such as tubular necrosis, proteinaceous casts in tubuli and medullary congestion, all of which were markedly improved by the higher dose of 17β-oestradiol. In addition, endothelin-1 content in the kidney after the ischaemia/reperfusion increased significantly by approx. 2-fold over sham-operated rats, and this elevation was dose-dependently suppressed by the 17β-oestradiol treatment. These results suggest that oestrogen exhibits protective effects against renal dysfunction and tissue injury induced by ischaemia/reperfusion, possibly through the suppression of endothelin-1 overproduction in postischaemic kidneys.

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