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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatocytes isolated from livers of rats with various models of acute uremia (binephrectomy, ureter ligation, uranyl nitrate-induced, or ischemic ARF) were incubated with glucagon, adrenalin, or cyclic AMP using serine as a substrate. A marked increase in glucose production was observed in the hepatocytes of uranyl nitrate-treated, binephrectomized, and ureter-ligated rats compared to starved controls or sham-operated animals. This effect was strengthened in the presence of glucagon, adrenaline, or cyclic AMP. In liver cells of binephrectomized and ureter-ligated animals, the production of acetoacetate and beta-hydroxybutyrate was significantly higher than in controls and sham-operated rats. Oxoglutarate and ATP production was only enhanced after ureter ligation. The correlation between glucose concentration and the cytosolic redox state was different in control and sham-operated rats than in either uremic group. This study confirms earlier investigations of a key role of serine in carbohydrate metabolism in acutely uremic rats.
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PMID:Effect of serine on gluconeogenic ability of hepatocytes in acute uremia. 633 Apr 26

Escherichia coli-induced pyelonephritis was studied in untreated alloxan-diabetic rats, insulin-treated diabetic rats, glucose water-drinking (diuresing) nondiabetic rats, and tap water-drinking (nondiuresing) nondiabetic rats following injection of E. coli either into the emptied urinary bladder, into the left kidney, or intravenously. For prevention of an ascending infection in the right kidney, the right ureter was ligated and transected immediately prior to bladder or intrarenal inoculation. These experiments established that in normal rats ascending renal infection alone occurred following introduction of small inocula into the bladder--and then only when facilitated by diuresis. In diabetic rats both ascending and hematogenous renal infection occurred following introduction of small inocula into the bladder. Insulin treatment that reduced hyperglycemia also reduced glycosuria and restored urinary antibacterial activity against small inocula of E. coli but only partially reduced polyuria and prevented hematogenous but not ascending infection. Thus, hyperglycemia was probably the major factor promoting hematogenous renal infection, whereas polyuria--and therefore vesicoureteral reflux--was the major factor promoting ascending infection.
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PMID:Effect of insulin treatment on the susceptibility of the diabetic rat to Escherichia coli-induced pyelonephritis. 638 97

Renal tubular function has been studied in pig fetuses of 105-112 d gestational age in new-born pigs 5-9 d old. The experiments were performed on anaesthetized animals, urines being collected by inserting a catheter into one ureter of the animal under study. The glomerular filtration rate was estimated and plasma concentrations and urinary excretion of the following substances were measured: sodium, potassium, calcium, ammonia, urea, phosphate, glucose fructose, creatinine, protein and exogenous 4-aminohippuric acid, and inulin. The reabsorption of water was considered in relation to the plasma vasopressin values. New-born pigs were loaded with glucose and fructose in order to determine the maximal tubular transport rate of these substances. Significant changes at birth occur in only a few functions of the tubulus system. Following delivery, major changes are: (1) the increased reabsorption of sodium and water which is probably the most important adaptation to extra-uterine life; (2) an apparent increasing impermeability of the tubular epithelium for creatinine, and (3) the direction of transport of fructose, which is reabsorbed by fetuses whereas neonates demonstrate a net secretion. Glucose and fructose are transported by different mechanisms. The experiments with fructose-loaded piglets demonstrate that there are at least two transport mechanisms for fructose: reabsorption - either passive or active - and secretion. The factors causing a shifting from one mechanism to the other are not yet known.
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PMID:Perinatal development of tubular function in the pig. 651 94

Liver cells were prepared from untreated controls, rats with various models of acute uraemia (uranyl nitrate-treated, bilaterally nephrectomised and ureter-ligated rats, rats with acute ischaemic renal failure) and sham-operated animals. Hepatocyte glucose output, pyruvate utilisation and lactate production were determined in the presence of Krebs-Ringer bicarbonate buffer with different pH values (7.1, 7.4, 7.6) using pyruvate, dihydroxyacetone, serine and fructose as substrates. In the presence of pyruvate and dihydroxyacetone a significant increase of glucose production in hepatocytes from bilaterally nephrectomised and ureter-ligated rats was observed. However, pyruvate-generated glucose production in the hepatocytes of uranyl nitrate-treated animals was unchanged, while a diminished glucose output was seen in the presence of dihydroxyacetone. A marked increase in glucose and lactate production in the presence of serine was observed in the hepatocytes of uranyl nitrate-treated, ureter-ligated and binephrectomised rats. However, lactate production from dihydroxyacetone in the liver cells of uranyl nitrate-treated animals was inhibited. In contrast to other types of uraemia, in acute ischaemic renal failure there is significantly lower hepatocyte glucose production using pyruvate as a substrate, but unchanged glucose generation from dihydroxyacetone or serine.
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PMID:The gluconeogenetic ability of hepatocytes in various types of acute uraemia. 681 Jan 92

Disturbances of carbohydrate metabolism during acute uraemia are characterized by the degradation of liver and muscle glycogen with a simultaneous activation of hepatic gluconeogenesis. After binephrectomy, the substitution of essential amino acids and keto analogues stimulate liver, but not skeletal muscle glycogen synthesis. Serine proves to be an optimal substrate for liver gluconeogenesis and muscle glycogen generation under acute uraemic conditions. Propranolol does not influence glycogenolysis of skeletal muscle in acutely uraemic rats. During starvation, acute uraemia leads to an increase of total carbohydrate content as well as of glycogen and glucose concentrations in heart muscle Alterations in carbohydrate contents are not observed in the kidney after ureter ligation. Enhanced glycogenolysis of skeletal muscle and liver during acute uraemia may be due to activation of phosphorylase kinase caused by the increased serum concentrations of various hormones (glucagon, catecholamines, parathormone) as well as free proteolytic activity, an increase of intracellular Ca2+-concentration and finally by alterations in the structure of contractile proteins.
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PMID:Carbohydrate metabolism and uraemia-mechanisms for glycogenolysis and gluconeogenesis. 745 93

Vascularized whole pancreas transplantation in the rat was performed on the abdomen using a cuff technique for vascular anastomoses. Two different exocrine drainage procedures, either intestinal or ureter drainage, were used. In the isograft transplant models, hyperglycemia was ameliorated immediately after transplantation and all of the grafts functioned during the observation period. In the allograft transplant models without immunosuppression, graft rejection, as defined by recurrence of hyperglycemia (blood glucose > 200 mg/dl) occurred 6-9 days post-transplant. Allograft rejection could be delayed approximately 1 month after transplant with short-term use of FK506. These different models, using either intestinal or ureter exocrine drainage, are similar to dominant clinical pancreas transplantation with enteric exocrine drainage or urinary tract drainage, respectively. It is thus concluded that whole pancreas transplant with either intestinal or ureter exocrine drainage is an ideal model for physiological and immunological experimental studies in pancreas transplantation.
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PMID:Experimental rat pancreas transplant: surgical technique and immunological considerations. 751 9

1. In the guinea pig isolated ureter, a maximally effective concentration of calcitonin gene-related peptide (CGRP, 0.1 microM) produced a prompt and transient suppression of myogenic phasic contractions (twitches) evoked by direct excitation (electrical field stimulation, EFS) of the smooth muscle. This suppressant effect is prevented by glibenclamide (1 and 10 microM), indicating the importance of K+ channel activation in its genesis. In the presence of either 1 or 10 microM glibenclamide, CGRP produced a partial (about 30%) and delayed inhibition of the evoked response, but failed to produce a full suppression of twitches. 2. The intensity and duration of the early, glibenclamide-sensitive suppressant effect of CGRP were inversely related to the frequency at which the ureters were driven by EFS. The glibenclamide-resistant inhibitory effect of CGRP was unaffected by changes in the EFS driving frequency, and cromakalim (3 microM) suppressed twitches independently of the EFS driving frequency. 3. Replacement of 80% glucose in the Krebs solution with 2-deoxyglucose (2-DOG) reduced the amplitude of the EFS-evoked twitches. In the presence of 2-DOG the inhibitory effect of CGRP was enhanced and prolonged when tested in the absence, but not in the presence, of glibenclamide. 2-DOG counteracted the inhibitory effect produced by increasing the EFS driving frequency on the response to CGRP. 4. In sucrose gap, both CGRP (0.1 microM) and cromakalim (3 microM) produced prompt hyperpolarization of the membrane. During continued superfusion for 15 min in unstimulated preparations, the hyperpolarizing effect of cromakalim and CGRP was sustained. When tested within 3 min from the end of 'exercise', induced by application of EFS at intervals of 15 sec for 30 min, the hyperpolarization by CGRP was reduced and shortened but that produced by cromakalim was unaffected. 5. These findings demonstrate that exercise and metabolic inhibition selectively influence, in opposite directions, the K+ channel opener action of CGRP in the guinea pig ureter, indicating that the ability of this neuropeptide to suppress latent pacemakers in smooth muscle is markedly dependent upon degree/frequency of cell activation. These results suggest that the ability of endogenous CGRP to suppress ureteral motility may be inversely related to the frequency of ureteral peristalsis, the effect being reduced by, for example, increase in diuresis.
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PMID:Effect of exercise and 2-deoxyglucose on the K+ channel opener action of CGRP in the guinea pig ureter. 874 2

We aimed at studying the mechanism(s) of the inhibitory effect exerted by calcitonin gene-related peptide (CGRP) on the spontaneous activity of the guinea-pig isolated renal pelvis. In organ bath experiments, CGRP (1-100 nM) produced a concentration-dependent (EC50 8 nM) partial inhibition (Emax about 35% inhibition of motility index) of spontaneous contractions. The potassium (K) channel opener, cromakalim (3-10 microM) promptly suppressed the spontaneous contractions in a glibenclamide-(10 microM) sensitive manner. Glibenclamide (10 microM) did not affect the inhibitory action of CGRP. The calcium (Ca) channel agonist, Bay K 8644 (1 microM), markedly enhanced the spontaneous activity of the renal pelvis and reduced the inhibitory effect of CGRP. The protein kinase A inhibitors Rp-cAMPS (300 microM), H8 (100 microM) and H89 (10 microM), and the blockers of intracellular Ca handling by sarcoplasmic reticulum, ryanodine (100 microM) and thapsigargin (1 microM) did not affect the response to CGRP. The response to CGRP was likewise unaffected by the nitric oxide synthase inhibitor, L-nitroarginine (30 microM) and by the protein kinase G inhibitor, KT5823 (3 microM). Furthermore, the inhibitory action of CGRP was not modified by lowering the extracellular concentration of K (from 5.9 to 1.2 mM) nor by increasing (from 2.5 to 3.75 mM) or decreasing (from 2.5 to 0.25 mM) the extracellular Ca concentration. Replacement of 80% glucose with 2-deoxyglucose (2-DOG) reduced the amplitude of spontaneous contractions, both in the absence and presence of 10 microM glibenclamide. In the presence of 2-DOG, the inhibitory action of CGRP was enhanced at a similar extent, either in the absence or presence of glibenclamide. In sucrose gap, the effect of CGRP (0.1 microM for 5 min) was separately analyzed in the proximal (close to the kidney) and distal (close to the ureter) regions of the renal pelvis. Both preparations discharged spontaneous (pacemaker) action potentials having different shape, duration and frequently. CGRP had no effect on pacemaker potentials in the proximal renal pelvis while producing about 30% reduction of the frequency of pacemaker potentials and motility index in the distal renal pelvis. Cromakalim (3 microM) abolished pacemaker potentials in both regions of the renal pelvis. In conjunction with the results of previous studies in the guinea-pig ureter, the present findings document the existence of remarkable regional differences in the effector mechanisms initiated by CGRP receptor occupancy in the guinea-pig pyeloureteral tract. CGRP appears to be inherently unable to activate glibenclamide-sensitive K channels in the guinea-pig renal pelvis, a mechanism which is central for its ability to suppress latent pacemakers in the ureter. Within the renal pelvis, the sensitivity to the inhibitory effect of CGRP appears in the more distal region, from which an 'ureter-like' action potential is recorded.
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PMID:CGRP inhibition of electromechanical coupling in the guinea-pig isolated renal pelvis. 875 Oct 82

An investigation of the functional and histological changes was done after en-bloc kidney-pancreaticoduodenal transplantation (kpdt) in the diabetes-induced, renal insufficient Lewis rats. For donor preparation, an end-to-side portocaval shunt was performed, and the aortic, vena caval segments, and ureter-bladder patch were obtained. They were anastomosed microsurgically to recipient's aorta, vena cava, and bladder in end-to-side fashion. Of 15 diabetes-induced kpdt rats, 14 survived. Two of the 14 surviving rats showed ischemic necrosis. The remaining 12 transplants showed well-preserved glomeruli and Langerhans islets for 5 months postoperatively. Biochemical data comparing diabetic and sham-operated rats (six rats each), six diabetic controls, and 12 kpdt rats showed no significant statistical difference at said observation period. The diabetes-induced kpdt rats showed improvement of following biochemical data: within 1 week postoperatively, the glucose level fell from 300 to 115 mg/dL; BUN level from >20 to <20 mg/dL; the creatinine level from 1.5 to <1.2 mg/dL. The insulin level returned to normal, 1.1 ng/mL, in 2 weeks. The results demonstrate that the kpdt model is an effective and successful operative technique in diabetic rats and may provide effective therapeutic methods for diabetes-induced renal insufficiency.
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PMID:Effects of simultaneous kidney-pancreaticoduodenal transplantation on diabetes-induced renal insufficiency in rats. 1149 88

This study was performed to investigate the impact of acute hyperglycemia (HG) on the permeability of the normal glomerular filtration barrier in vivo. In anesthetized Wistar rats (250-280 g), the left ureter was catheterized for urine collection, while simultaneously blood access was achieved. Rats received an intravenous (iv) infusion of either 1) hypertonic glucose to maintain blood glucose at 20-25 mM (G; n = 8); 2) hypertonic glucose as in 1) and a RhoA-kinase inhibitor (Y-27632; Rho-G; n = 8); 3) 20% mannitol (MANN; n = 7) or 4) hypertonic (12%) NaCl to maintain plasma crystalloid osmotic pressure (pi(cry)) at approximately 320-325 mosmol/l (NaCl; n = 8) or 5) physiological saline (SHAM; n = 8). FITC-Ficoll 70/400 was infused iv for at least 20 min before termination of the experiments, and plasma and urine were collected to determine the glomerular sieving coefficients (theta) for polydisperse Ficoll (molecular radius 15-80 A) by high-performance size-exclusion chromatography. In G there was a marked increase in for Ficoll(55-80A) at 20 min, which was completely reversible within 60 min and abrogated by a Rho-kinase (ROCK) inhibitor, while glomerular permeability remained unchanged in MANN and NaCl. In conclusion, acute HG caused rapid, reversible increases in for large Ficolls, not related to the concomitant hyperosmolarity, but sensitive to ROCK inhibition. The changes observed were consistent with the formation of an increased number of large pores in the glomerular filter. The sensitivity of the permeability changes to ROCK inhibition strongly indicates that the cytoskeleton of the cells in the glomerular barrier may be involved in these alterations.
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PMID:Acute hyperglycemia induces rapid, reversible increases in glomerular permeability in nondiabetic rats. 2023 33


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