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

Although epinephrine stimulates insulin release by activation of beta-adrenergic receptors, its dominant effect (mediated by stimulation of alpha-adrenergic receptors) is an inhibition of insulin secretion that is powerful enough to suppress the secretory activity of insulin's most potent stimulants. The insulin-secretory response to potassium chloride (KCl) infusion, however, is not suppressed; in fact, in ureter-ligated dogs simultaneously infused with 360 microgram. epinephrine per hour and 2 mEq. KCl per kilogram per hour, insulin release is actually increased about threefold (over controls). Propranolol blockade of beta-adrenergic receptors essentially abolishes the insulin response to KCl infusion, with and without epinephrine. It is unlikely that KCl, like epinephrine, provokes insulin release by direct stimulation of the beta-adrenergic receptors of the beta cells of the pancreatic islets. However, potassium in some way enhances the beta adrenergic (secretory) activity of epinephrine and blunts its usually dominant alpha-adrenergic (inhibitory) effect.
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PMID:Epinephrine enhancement of potassium-stimulated immunoreactive insulin secretion. Role of beta-adrenergic receptors. 20 80

In anuric dogs loaded with K by infusion with 2 meq KCl/kg per h until prelethal hyperkalemic cardiotoxicity appears, the extent of transmembrane K transfer depends on the origin of the anuria. Animals with bilateral ureter ligation transfer a mean of 1.2 meq/kg to intracellular fluid, while those with bilateral nephrectomy transfer more than 2.5 times as much (3.1 meq/kg). Further, if dogs with functioning kidneys are ureter ligated or nephrectomized after approximately 45 min of K loading, K transfer ultimately falls as infusion continues. The fall is precipitate and over 90% in ligated animals; but it is gradual, and only 10% in those that are nephrectomized. Finally, K transfer, because of the absence of insulin, is negligible in K-loaded pancreatectomized dogs with bilateral ureter ligation, but fairly substantial in pancreatectomized animals with bilateral nephrectomy. The data suggest that ureter ligation and hyperkalemia activate a renal mechanism that interferes with the transfer of infused K to intracellular fluid. The mechanism may involve the renin-angiotensin II-aldosterone system to a limited degree.
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PMID:Inhibition of transmembrane K transfer in ureter-ligated dogs infused with KCl. 99 Jan 4

The role of renal tubules was explored by two kinds of experiments: (1) inhibition of the tubular reabsorption of insulin by induced polyuria; (2) suppression of insulin filtration by ureter clamping; 1. Anaesthetized dogs maintained in normoglycaemia by glucose compensation were infused with crystalline and 125I-insulins. Polyuria was induced by: (1) saline-bicarbonate infusion; (2) furosemide with saline-bicarbonate infusion to replace urine losses; (3) massive infusion of mannitol. Inulin and paraminohippuric acid were used to estimate the glomerular filtration rate and the renal plasma flow. The permeability of the glomerular wall (pore radius and total area of the pores per unit of path length) was determined by measuring the sieving curve of 131I-polyvinyl-pyrrolidone fractions during basal and treatment periods. Mannitol infusion was able to bring the insulin/inulin clearance ratio up the values of the sieving coefficient of insulin (insulin filtration rate) without modifying the permeability of the glomerular wall; saline infusion displayed a similar effect; furosemide, only a minute one although it induced a more marked polyuria. 2. Clamping of the left ureter was performed on dogs with catheters inserted into the artery, the left renal vein, the pelvis and a renal lymphatic vessel. Almost complete suppression of the glomerular filtration was achieved. It slightly increased the high insulinic concentration of the renal lymph, entailed a 1/3 decrease in the extraction ratio of insulin and reduced by half its renal clearance. In conclusion, the tubules participate to the catabolism of insulin by two different mechanisms: (1) an uptake from the tubular fluid which can be inhibited by diuretics exerting their main action on the proximal tubules; (2) a direct catabolism from the interstitial fluid resulting from the large permeability of the peritubular capillaries to insulin.
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PMID:The participation of the renal tubules to the metabolism of insulin. 100 Oct 4

In order to determine the major routes of insulin degradation in the body, insulin was labelled with a 'trapped' or 'residualizing' label: [125I]tyramine-cellobiose ([125I]TC) and injected intravenously in dogs. In contrast to conventional iodine-labelled insulin (131I-insulin), the [125I]TC-insulin allows measurements of total uptake in specific organs in vivo because the radioactive degradation products do not leave the cells. One h after the injection of trace doses, the amount of radioactivity recovered in the kidney from [125I]TC-insulin was nine times higher than when conventional [131I]insulin was used. In the blood, the amount of acid-precipitable radioactivity was the same for both labelled preparations, indicating similar clearance rates. A comparison of the uptake of insulin in filtering vs. non-filtering (ureter-occluded) kidneys indicated that the uptake of insulin is twice as high through the luminal than through the basolateral cell membrane; after 60 min, 8.9 +/- 0.8% of the injected [125I]TC-insulin dose remained in the filtering kidney and 3.2 +/- 0.2% of the dose was accumulated in the contralateral kidney, with occluded ureter but normal blood perfusion. In both filtering and non-filtering (ureter-occluded) kidneys, the subcellular distributions of [125I]TC-insulin were studied after various times by isopycnic sedimentation in sucrose gradients. No difference between peritubular and tubular uptake was discernible. The intracellular transport was rapid, leading to accumulation of radioactive label in dense lysosomes within 10 min.
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PMID:Luminal and basolateral uptake and degradation of insulin in the proximal tubules of the dog kidney. 144 37

A man aged 46 years with diabetes mellitus was admitted with acute right-sided renal symptoms. Pyelonephritis emphysematous without concretions was found. The patient was treated with insulin, fluids, electrolytes and antibiotics and nephrostomy was performed and, subsequently, an internal JJ-catheter in the ureter. The symptoms disappeared and he was discharged on a low dosage of sulphamethizol. After the planned removal of the JJ-catheter, sepsis running a lethal course developed. This emphasizes the importance of adequate prophylactic antibiotic therapy in connection with interventions in the urinary tracts.
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PMID:[Fatal emphysematous pyelonephritis]. 163 72

In vitro tissue culture techniques were employed to study the effects of bacterial endotoxins on the growth of normal epithelial cells from the human ureter (NHU). Primary cultures of NHU cells were initiated from explant outgrowth cultures of human ureteral tissue and cultured on collagen gel in F-12* medium containing 1% fetal calf serum (FCS). Optimal clonal growth of secondary cultures of NHU cells seeded at relatively low seeding cell densities, directly on plastic dishes, was achieved in F-12* medium containing bovine pituitary extract (0.5% BPE) and 0.05% BSA. Results indicated that insulin in the F-12* medium could be replaced by three orders of magnitude less IGF-1. Further clonal growth experiments demonstrated that PGE1 is growth stimulatory and can replace BPE as a growth factor requirement. This finding was in agreement with the fact that BPE growth requirement could be replaced by cholera toxin or dibutyryl cAMP. These results suggested that both BPE and cholera toxin operated by activation of a cAMP-dependent mitogenic pathway. Seven gram-negative bacterial lipopolysaccharides (LPS) and three gram-positive bacterial lipotechoic acids (LT) were tested for their effects on NHU clonal growth. Three out of the five LPS derived from Escherichia coli (strains 055:B5, 0128:B12, and 0127:B8), LPS from Klebsiella pneumoniae, and LPS from Pseudomonas aeruginosa all showed significant growth inhibitory effects at minimally effective doses ranging from 5 to 25 micrograms/ml. LPS derived from E. coli strain (0111:B4) had no growth effects at the highest concentration tested (100 micrograms/ml). In contrast, LT derived from Streptococcus pyogenes, S. faecalis, Staphylococcus aureas, and Bacillus subtilis all markedly enhanced clonal growth at concentrations ranging from 1 microgram/ml less than [LT] less than 50 micrograms/ml. LT from Strep. pyogenes was inhibitory to clonal growth at 100 micrograms/ml. The growth inhibitory effects of LPS were shown to be sensitive to the presence of hydrocortisone in the growth medium, indicating that LPS effects on growth are mediated via the arachidonic acid cascade. We speculate that these results indicate a link between the susceptibility of uroepithelial tissue to the pathogenic microflora seen in urinary tract diseases and the differential sensitivity of proliferation-competent uroepithelial cells to growth inhibition by LPS produced by gram-negative bacteria. However, further studies with uropathogenic serotypes will be necessary to corroborate this possibility. The growth-stimulating activity of LTs produced by gram-positive bacteria may be due to their ability to bind to cell-associated fibronectin and to activate the fibronectin receptor as part of ligand receptor-induced mitogenic transmembrane signalling pathway.
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PMID:Effects of growth factors, hormones, bacterial lipopolysaccharides, and lipotechoic acids on the clonal growth of normal ureteral epithelial cells in serum-free culture. 173 Jul 86

Differentiation of the metanephrogenic mesenchyme is triggered by an inductive tissue interaction between an inducer tissue and the mesenchyme. It is generally believed that the epithelial ureter bud acts as an inducer during in vivo development. In response to the inductive stimulus most of the mesenchymal cells convert into epithelial cells, while a small fraction differentiates into stromal cells. In vitro, differentiation of isolated mesenchyme to epithelium can be induced by a variety of embryonic tissues, but nothing is known about the molecular nature of the inducing stimulus. In recent years, large numbers of polypeptide growth factors have been described, which in addition to proliferative effects were shown to exert effects on a variety of biological phenomena such as chemotaxis, inflammation, tissue repair, or induction of embryonic development. We therefore analyzed whether growth factors in the absence of inducer tissue can induce isolated kidney mesenchyme to differentiate into epithelium or interstitium. As expected, both growth and differentiation into epithelium were stimulated by an inducer tissue, the spinal cord. We found that none of the various growth factors tested (including epidermal growth factor, transforming growth factors alpha and beta, insulin-like growth factors I and II, fibroblast growth factor, platelet-derived growth factor, and retinoic acid) could mimick the effect of an inducer tissue, although we tested the factors over a wide concentration range. One of the tested factors, epidermal growth factor (EGF) stimulated the mesenchymal cells to become stromal cells, although it could not stimulate development into epithelium. EGF could stimulate stromal development both when the mesenchyme was cultured in isolation and when the mesenchyme was stimulated by an inducer tissue to become epithelium. The expansion of the stromal compartment in response to EGF treatment occurred at the expense of the epithelial cells, but EGF could not completely suppress the formation of epithelium. These data suggest the presence of EGF receptors in the developing kidney, but since application of soluble EGF leads to abnormal development, soluble EGF cannot be the natural ligand. We suggest that locally produced mitogens with an EGF-like structure may regulate the relative amounts of stroma (interstitium) and epithelium in the developing kidney.
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PMID:Development and growth of mouse embryonic kidney in organ culture and modulation of development by soluble growth factor. 201 31

Ureter ligated control dogs that are K loaded by infusion with 2 mEq KCl/kg.h until prelethal electrocardiographic changes of hyperkalemic cardiotoxicity appear, transfer somewhat more than half the K load to intracellular fluid. The proportion is not significantly changed by adrenalectomy, but increased by treatment with aminophylline; the treatment has no effect on K transfer in adrenalectomized animals. Insulin is not involved; in dogs with adrenalectomy and pancreatectomy treatment with pharmacological dosages of adrenaline (Abbot), beta agonist activity is as effective as that with aminophylline. We conclude that aminophylline improves K transfer, by investifying beta agonist activity of endogenous adrenaline; it is known that increased beta agonist activity enhances beta receptor mediated K transfer in K loaded ureter ligated, intact and adrenalectomized dogs.
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PMID:Aminophylline activation of adrenaline mediated transmembrane K transfer in hyperkalemic dogs. 227 Oct 6

The renal disposition of insulin in acute renal failure has not been evaluated. We used the isolated perfused rat kidney to test the hypothesis that acute renal failure (ARF) decreases renal insulin clearance. We used warm ischemia for 45 min, uranyl nitrate 5 mg/kg, ureter ligation, and nonfiltering kidneys as methods of inducing ARF. Comparisons were made with normal control kidneys. The concentrations of insulin in perfusate and urine was determined by radioimmunoassay. Acute renal failure caused significant reductions in glomerular filtration rate, sodium and potassium reabsorption, and an increased urine pH. Warm ischemia and uranyl nitrate toxicity caused a 50% decrease in the renal clearance of insulin. Nonfiltering kidneys cleared insulin at a rate 90% decreased from controls. Ureteral ligation caused a 32% decrease in insulin clearance. Filtration was necessary for insulin to be cleared from perfusate. We conclude that ARF decreased renal insulin clearance through a decrease in insulin uptake from both the tubular lumen and peritubular surface.
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PMID:Effect of acute renal failure on insulin disposition in the isolated perfused rat kidney. 331 99

In ureter ligated dogs intravenous administration of KCl stimulates both insulin secretion and activity of a kaluresis independent K homeostatic mechanism (K transfer capacity) that retards the development of hyperkalemia by transferring K to intracellular fluid. If the preparation is K loaded by infusion with 2 mEq KCl/kg/hr until prelethal ECG changes of hyperkalemic cardiotoxicity appear, about 50% of administered K is transferred. An increased proportion--70%--is transferred if the animal is K loaded 70 minutes after pancreatectomy--when serum immunoreactive insulin is fixed at less than 4 uU/ml. That proportion (70%) is unchanged by simultaneous adrenalectomy, but is reduced to less than 40% by propranolol blockade of B receptors. Increased post pancreatectomy K transfer capacity apparently involves K transfer mediated by B receptors that are activated by an extra-adrenomedullary B agonist(s). Findings also indicate that residual post pancreatectomy insulin biological activity mediates K transfer.
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PMID:Kaluresis independent K homeostasis in dogs: activity after ureter ligation and pancreatectomy. 362 19


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