Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparative study on the kidney of Pulmonata living on land (Stylommatophora) and in fresh water (Basommatophora) was made. The sections performed in three different planes allowed us to know the 3-dimensional pattern of its components: renopericardial duct, kidney sac and ureter. Renopericardial duct runs far into the kidney sac. The duct of Basommatophora is longer and bears also longer cilia than that of Stylommatophora. Kidney sac is similar in both groups and is made up of a wall from which a complex lamellar system spreads into the cavity. Lamellae are longer and more numerous at the dorsal wall, being the lumen of the organ eccentric. The cavity is lined by columnar epithelial cells (nefrocytes) with brush border. Characteristic of the nefrocytes is the presence of a large apical vacuole containing an excretion granule. In Lymnaea there are also lamella lined by cubic epithelium without excretion granule. The union between kidney sac and ureter is different from one another in the three species studied. In Lymnaea the kidney sac narrows and forms the ureter; the connexion in Cryptomphalus is achieved through a 200 micrometer window; and in Helicella there is a duct between both parts. The ureter has a columnar epithelium with very deep infoldings of the basal cell membrane, according to its osmotic regulative function. In Stylommatophora there are primary and secondary ureters, while in Basommatophora there is only one type.
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PMID:[Excretion in basommatophora and stylommatophora pulmonata (author's transl)]. 72 32

This study explores the role of brush border (luminal) membranes in p-aminohippurate (PAH) transport by the rabbit kidney. Under control conditions PAH appears in urine at the same rate as simultaneously injected inulin; no evidence for a secretory delay was found. After suppression of secretion by limiting concentrations of Benemid (probenecid), urinary PAH is largely derived from glomerular filtrate: its tubular transit time exceeds that of inulin. Excess Benemid abolishes this delay. Filtered PAH on its way to excretion appears to be permitted by a mechanism sensitive to high concentrations of Benemid to pass through an extraluminal volume equivalent to that of the proximal tubule cells. These results strengthen the previously suggested model for tubular PAH transport, and provide justification for use of glomerulus-to-ureter transit times in localizing tubular transport mechanisms.
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PMID:Movement of p-aminohippurate between lumen and cells of renal tubule. 87 Nov 64

Renal cortex homogenates from aged (greater than 5 y) rabbits showed decreased specific activities of brush border membrane enzymes compared to those from control young (6 m) rabbits but the specific enzyme activities of basolateral membrane, endoplasmic reticulum and mitochondria did not differ between the two groups. The stimulatory effects of parathyroid hormone (PTH) on the Ca(2+)-pump enzyme [(Ca(2+)+Mg2+)-ATPase] activity in kidney cortex homogenates were markedly less in aged rabbits, but the effect of cAMP on this enzyme activity was similar. Moreover, the production of cAMP induced by PTH was markedly less in the renal cortex homogenates from aged rabbits. From these results, we have proposed the following mechanism; aging--decrease in the response of cAMP to PTH in renal cortex--decrease in the stimulatory effect of PTH via cAMP on the Ca(2+)-pump enzyme--decreased reabsorption of Ca2+ from ureter--increased urinary Ca2+ secretion. This pathway may contribute to the worsening of senile osteoporosis.
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PMID:Effects of aging on renal response to parathyroid hormone in vitro. 135 71

To clarify the routes for renal methylmercury uptake, the effects of ureter ligation and pretreatment of probenecid, an organic anion transport inhibitor, or acivicin, a gamma-glutamyltranspeptidase (gamma-GTP) inhibitor, on renal methylmercury content were investigated in mice. For 120 min after CH3HgCl (5 mumol/kg, i.v.) injection, renal methylmercury content in bilateral ureter-ligated mice was approximately 50% lower than that of sham-operate mice. The glomerular filtration rate was reduced to about 15% of the control by ureter ligation. These results suggest an important role of glomerular filtration in the renal methylmercury uptake. Pretreatment with probenecid (0.5 or 1.0 mmol/kg, i.p.) reduced the renal methylmercury accumulation 30 min after CH3HgCl injection in a dose-dependent manner in both ureter-ligated and sham-operated mice. Urinary methylmercury excretion was not affected by probenecid pretreatment. Renal methylmercury content of ureter-ligated mice was not changed by pretreatment with acivicin (0.5 or 1.0 mmol/kg. i.p.), which was previously reported to decrease the renal methylmercury content in mice. Coadministration of GSH (10 mumol/kg, i.v.) with CH3HgCl increased the renal methylmercury uptake determined 5 min after injection in ureter-ligated mice. These results suggest that at least two transport systems play major roles in renal methylmercury uptake: one is a route from the glomeruli through the brush border membrane which is dependent on the action of gamma-GTP, and the other route is the one using an organic anion transport system through the basolateral membrane.
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PMID:Routes for renal transport of methylmercury in mice. 139 70

Enzyme histochemistry was assessed in semi-thin glycolmethacrylate sections after 100 mg/kg 2-bromoethanamine (BEA) hydrobromide had been given ip to male Wistar rats to induce renal papillary necrosis. Changes in the proximal tubular marker enzymes alkaline phosphatase (Alk Phos), gamma-glutamytranspeptidase (GGT) and adenosine triphosphatase (ATPase) were not apparent before 8 hr, but there was a progressive loss up to 144 hr. The proteinaceous PAS-positive casts in the loops of Henle and the collecting ducts stained for Alk Phos and GGT (from 12 hr) and for ATPase (from 18 hr). Acid phosphatase (Acid Phos) staining was increased in the proximal tubule lysosomes from 18 hr. There was a marked increase in Alk Phos in all hyperplastic upper urothelial cells from 8 to 24 hr, and a mosaic of staining remained in the pelvis adjacent to the necrosed papilla at 144 hr. At 12 hr, there was an increase in the staining of the pelvic, ureter and bladder vascular endothelial ATPase, the intensity and area of which increased progressively from 18 hr and almost occluded the capillary lumens in the worst affected areas by 144 hr. These data show several distinct series of pathological changes after the administration of BEA. The subtle degenerative changes in the proximal tubule followed the papillary lesion, but exfoliated brush border and proximal tubular cells were important components of the protein casts in the distal nephron. Similarly, the intense Alk Phos staining in the hyperplastic regions of the upper urothelium and the increased pelvic, ureteric and bladder endothelial ATPase staining suggested they develop as a consequence of the papillary lesion.
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PMID:Enzyme histochemical changes in an acutely induced renal papillary necrosis. 197

The construction of renal lobules in Triturus (Cynops) pyrrhogaster was studied by reconstruction from serial semithin sections, and the structure of nephrons, collecting ducts and ureters was investigated by means of light and electron microscopy. In T. pyrrhogaster the kidney was mesonephros in construction; renal lobules were arranged segmentally and each of them sent one ureter. Male ureters ran caudally and met together before joining the Wolffian duct. In renal lobules, long collecting ducts ran medio-laterally in the dorsal aspect of the kidney and sent several branches ventrally. Each branch duct or short collecting duct received one nephron. Each nephron had five segments; 1) renal corpuscle, 2) ciliated neck segment with or without a naphrostome, 3) proximal tubule, 4) ciliated intermediate segment and 5) distal tubule. Proximal and distal tubules were segregated spacially in renal lobules and occupied the peripheral and central zone respectively. The filtration barrier of the glomerulus consisted of both the basal lamina of podocytes and the subendothelial connective tissue, and was much thicker than the mammalian filtration barrier. Proximal tubule cells had a brush border, apical specialization for reabsorption of organic materials and well-developed smooth endoplasmic reticulum, but few baso-lateral interdigitations. In distal tubule cells, baso-lateral interdigitations and infoldings were well-developed. Collecting duct cells had a sparse cytoplasm. Ureter cells in males contained many secretory granules. On the basis of structural organization of the newt kidney as well as physiological data in literature, we suggest that in land vertebrates proximal tubules were primarily adapted to reabsorption of organic materials and distal tubules to reabsorption of electrolytes and water.
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PMID:The structure of the kidney of Japanese newts, Triturus (Cynops) pyrrhogaster. 683 32

The influence of unilateral ureteral ligation in the rat nephron has been morphometrically analysed. The glomeruli show no significant differences compared with the control groups. The lumen of the tubulus rectus I increases significantly, but irregularly, after the 6th day of ureter ligation. The brush border is mostly destroyed after the 8th day. The tubulus rectus II changes only very little during this period. At the beginning of the ligation the lumen dilates, and at the end of the experiment the tubulus becomes normalised. The most important changes have been seen on the collecting tubules. As a consequence of increased intratubular pressure the lumina continuously dilate.
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PMID:[Studies of the morphological and morphometrical changes in the rat nephron after unilateral ureteral ligation (author's transl)]. 739 30

The mechanisms underlying the inhibitory effects exerted by probenecid and cimetidine on the renal excretion of 3'-azido-3'-deoxythymidine (AZT) were investigated in rats in vivo. On i.v. administration, the findings indicated that both probenecid and cimetidine increased the plasma concentration of AZT and inhibited its renal excretion. To clarify the mechanisms underlying the interaction of these drugs with AZT and to elucidate the process of renal secretion of AZT, further investigation was performed, in which [3H]AZT (0.5 microM) was injected rapidly into the right renal artery, and its outflow profile from the right ureter was compared with that from the left ureter. In control experiments, 56.6% of the administered AZT was secreted from the right kidney, and it was calculated that the transcellular transit time of AZT in this process was 0.30 min. In the presence of 10 mM probenecid and of 10 mM cimetidine, the secretion of AZT was reduced to 15.3 and 32.3%, respectively, the inhibition induced by probenecid being more effective than that induced by cimetidine. However, the transcellular transit time of AZT increased to 0.53 and 1.21 min in the probenecid and cimetidine studies, respectively. Thus, cimetidine was more potent than probenecid in its effects on the transit time. These findings indicate that probenecid and cimetidine affect different steps in the renal secretion of AZT. It was therefore concluded that, on the renal plasma membrane, AZT is transported by anion transport systems, whereas on the brush border membrane, AZT is secreted by cation transport systems.
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PMID:Effects of probenecid and cimetidine on the renal excretion of 3'-azido-3'-deoxythymidine in rats. 781 70

To clarify the mechanism of mobilization of renal and hepatic cadmium (Cd) by N-benzyl-D-glucamine dithiocarbamate (BGD) and N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD) in mice exposed to Cd, the effects of pretreatment with probenecid, an organic anion transport inhibitor, or with acivicin, a gamma-glutamyltranspeptidase (gamma-GTP) inhibitor and ureter-ligation were investigated on the excretion and distribution of chelating agents and Cd. The renal contents of BGD and HBGD were increased by ureter-ligation and decreased by acivicin pretreatment. The mobilizing effect of BGD on the renal Cd was inhibited by probenecid pretreatment. The action of HBGD in removing Cd from the kidney was inhibited by both probenecid pretreatment and ureter-ligation. These results suggest that BGD and HBGD are mainly taken up into the renal tubular cells through the basolateral membrane which is dependent on the action of gamma-GTP; that the Cd-BGD complex formed in the tubular cells is secreted by a probenecid-sensitive organic anion transport system through the basolateral membrane; and that the Cd-HBGD complex formed in the tubular cells is secreted to the tubular lumen by an organic anion transport system through the brush border membrane. Probenecid pretreatment increased the hepatic contents of BGD and HBGD and also promoted the effects of these chelating agents in removing Cd from the liver, indicating an inhibitory effect of probenecid on the glucuronidation of BGD and the secretion of HBGD from the kidney. These results suggest that BGD and HBGD are taken up into the liver and secreted from the organ to the bile by a transport system other than a probenecid-sensitive transport mechanism.
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PMID:Mechanism of mobilization of renal and hepatic cadmium by dithiocarbamates in mice. 790 46

Two possible sites of renal metabolism exist: intracellular, by enzymes within the peritubular cells, and intraluminal, by ecto-enzymes embedded on the brush border membrane. The esterolysis of enalapril to its dicarboxylate metabolite, enalaprilat, was studied in the isolated perfused, nonfiltering rat kidney preparation (NFK) and compared with that observed for the isolated perfused rat kidney (IPK) to ascertain the site of metabolic conversion. For the NFK, filtration was obliterated with the high oncotic pressure (8% bovine serum albumin in plasma) and ligation of the ureter, thus preventing enalapril from reaching intraluminal sites by filtration. The steady-state renal plasma clearance of enalapril in the NFK was 2.0 ml/min/g, a value similar to that (2.1 ml/min/g) observed previously for the IPK. The rate of appearance of enalaprilat, the metabolite, in venous plasma for the NFK (30 +/- 3% of the input rate of enalapril) was also comparable with that for the IPK (27 +/- 4%). Further, identification of the site of enalapril metabolism (cellular or luminal) was aided by simulations based on physiological models and parameters obtained previously on the renal handling of enalapril and enalaprilat. These parameters were optimized to match closely the experimental observations. The predicted total and metabolic renal clearances for the IPK or for the NFK were similar for both the "cellular model" and "luminal model": in both instances, values for the NFK were 59-65% of those for the IPK. By contrast, predictions for the venous output rate of enalaprilat (as a percent of the input rate of enalapril) were different: the "cellular model" predicted no change in value between the NFK and the IPK, whereas metabolite appearance was greatly magnified for the NFK (289% that of the IPK) with luminal metabolism. The lack of difference in venous outflow of enalaprilat for the NFK and IPK was more congruent with the notion of intracellular and not intraluminal esterolysis of enalapril.
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PMID:Intracellular and not intraluminal esterolysis of enalapril in kidney. Studies with the single pass perfused nonfiltering rat kidney. 953 19


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