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)

P-fimbriated Escherichia coli, which cause nonobstructive pyelonephritis, adhere to a specific urothelial glycolipid receptor. In either the presence or absence of reflux (in the area of turbulent urine flow) these bacteria ascend the ureter and cause a decrease in ureteral motility. Endotoxin causes peristalsis to cease, leading to ureteral dilatation and change in papillary shape, thus allowing intrarenal reflux and adherence of the bacteria to renal tubules. Bacterial infection of a refluxing ureter may cause reflux to persist. Once the bacteria reach the kidney rapid effects occur at the cellular level with activation of complement followed by granulocytic aggregation and capillary obstruction, causing renal ischemia and damage during reperfusion. In addition, during phagocytosis the respiratory burst occurs, releasing toxic oxygen molecules, which leads to renal tubular death, invasion of the interstitium, microabscess and renal scar formation, that is chronic pyelonephritis, which equates with reflux nephropathy.
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PMID:Vesicoureteral reflux and pyelonephritis in the monkey: a review. 143 97

The effects of stimulation of renal mechano- and chemoreceptors on the afferent renal nerve activity (ARNA) were observed in 44 anesthetized rabbits. The results obtained were as follows: (1) Elevation of ureteral pressure (UP) could induce an increase in integral value of ARNA by 175.13 +/- 22.41% (P less than 0.001). (2) KCl (0.15 mol/L) and NaCl (1 mol/L) perfused retrogradely into pelvis via ureter route resulted in increase of integral value of ARNA by 253.79 +/- 21.64% and 172.17 +/- 15.19% (P less than 0.001), respectively. (3) Four patterns of afferent unit discharge were found: no spontaneous activity, regular spontaneous activity, regular spontaneous activity with burst and irregular spontaneous activity. (4) The units of afferent renal nerve with no spontaneous activity were activated markedly by elevation of UP, while the units with spontaneous activity showed no change. (5) In response to the retrograde perfusion of KCl (0.15 mol/L) and NaCl (1 mol/L) into pelvis, the activity in units with spontaneous discharge increased markedly by 210.70 +/- 23.40% and 140.07 +/- 15.72% (P less than 0.001), respectively, and the other units may be recruited concomitantly. (6) The units with no spontaneous discharge were activated by renal artery occlusion. The results implied that there are mechanoreceptor, R1 and R2 chemoreceptors in the kidney of the rabbit, and they may sense the change in UP, renal ischemia and ionic (K+, Na+) concentration of the solute within pelvis.
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PMID:[Observation on the afferent nerve activity induced by stimulation of renal receptors in the rabbits]. 208 72

Renal ischemia was produced in anesthetized rats by a bilateral ligation of the renal artery, vein, and ureter. Pretreatment with hydralazine (0.3-10.0 mg/kg i.v.) resulted in a dose dependent reduction in elevated plasma creatinine levels 24 hr after a 60 min ischemic episode, indicating a protective effect on post-ischemic renal function. Hydralazine (3.0 mg/kg, i.v.) produced a fall in arterial blood pressure and exaggerated and/or extended post-ischemic depressions in renal blood flow, renal transport activity (in vitro para-aminohippurate uptake) and renal ATP levels. These results indicate that the hypotensive activity of hydralazine may have indirectly benefited the post-ischemic kidney by prolonging a relative anoxic condition which possibly allowed renal cells to recover under conditions where minimal tubular activity was present.
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PMID:Protective effects of hydralazine in a renal ischemia model in the rat. 360 Jan 94

This study was designed to test the hypothesis that high renal levels of adenosine (ADO) may alter glomerular filtration rate (GFR) control by angiotensin II (ANG II). In normal kidneys, ANG II infusion (20 ng X kg-1 X min-1 iv) decreased renal blood flow (RBF) to 61 +/- 3% of control, increased filtration fraction (FF) to 173 +/- 21% of control, and did not change GFR significantly. During intrarenal ADO infusion at a rate of 1.0 mumol/min, ANG II (20 ng X kg-1 X min-1 iv) decreased RBF and GFR to 61 +/- 5 and 64 +/- 6% of control, respectively. After blocking changes in tubuloglomerular feedback by occluding the ureter during mannitol diuresis, ANG II increased stop-flow pressure and postglomerular resistance (RPG) markedly but did not alter preglomerular resistance (RA), suggesting that the direct actions of circulating ANG II are confined primarily to efferent arterioles in the absence of changes in tubuloglomerular feedback. However, during intrarenal ADO infusion and inhibition of tubuloglomerular feedback, ANG II decreased stop-flow ureteral pressure and raised RA and RPG to 213 +/- 27 and 155 +/- 7% of control, respectively, while decreasing RBF to 59 +/- 5% of control. These observations suggest that ADO markedly alters the control of GFR by ANG II, possibly by causing ANG II to constrict preglomerular vessels, an effect that is not apparent in most physiological conditions but which could play a role in lowering GFR when renal ADO and ANG II levels are both elevated, as in severe renal ischemia.
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PMID:Adenosine alters glomerular filtration control by angiotensin II. 370 43

This study examined the possibility that the renal tubules are the site of the sensors that respond to renal artery stenosis (RAS) and which initiate the events leading to pressor hyperresponsiveness. A nonfiltering kidney (NFK) was produced in 32 rabbits by 2 hr of total renal ischemia plus permanent ligation of the ureter; the opposite kidney remained undisturbed. Sixteen of these rabbits also received RAS of the NFK. An additional 16 rabbits received RAS without production of a NFK, and 16 more rabbits were sham-operated controls. In acute experiments 3 days later in conscious rabbits, infusions of norepinephrine at several doses resulted in greater increases in mean arterial pressure in the RAS rabbits, with filtering kidneys (2-K, 1-clip) and with NFKs (2-K, 1-clip with NFK), than in the NFK rabbits without RAS (2-K control with NFK) or in the control rabbits (2-K control). Measurements of cardiac output revealed greater increases in total peripheral resistance as well as in mean arterial pressure in response to norepinephrine in the RAS rabbits both without and with a NFK. Because production of a NFK in rabbits did not prevent the development of pressor and vascular hyperresponsiveness 3 days after RAS, these studies indicated that the renal sensors that detect changes in the kidney following RAS and which initiate the series of events leading to pressor and vascular hyperresponsiveness, probably are not located in the renal tubules.
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PMID:Pressor and vascular responsiveness in renal prehypertensive rabbits with a nonfiltering kidney. 389 87

This study tested the ability of the converting enzyme inhibitor, captopril, to lessen the severity of acute renal failure following temporary occlusion of the renal artery. In the control group, 11 dogs were anesthetized with halothane, and the left kidney was isolated through a midline incision. The renal artery, vein, and ureter were then clamped for 120 min. Immediately after occlusion, the kidney was flushed with 40 ml of saline at 34 degrees C. When the clamp was released, a contralateral nephrectomy was performed and the animal allowed to recover. Serum creatinine and blood urea nitrogen levels were followed on a daily basis thereafter. Thirteen captopril-treated dogs were treated in the same fashion except that captopril (1.25 ml/kg, i.v.) was given prior to the 120-min period of renal ischemia. Three of 11 (27%) control dogs survived, whereas 10 of 13 (77%) captopril-treated animals survived (P less than 0.05). Serum creatinine (5.4 +/- 2.5 mg/dl) and serum urea nitrogen (96 +/- 33 mg/dl) peaked on day 8 in the captopril-treated group and were consistently lower than in the untreated group. These observations suggest that captopril is useful when temporary interruption of the renal circulation is encountered, such as in renal autotransplantation, cadaveric renal transplantation, and renal revascularization. These data also suggest that inhibition of the renin-angiotensin system may lessen the severity of acute renal failure following renal ischemia.
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PMID:Enhancement of recovery in postischemic acute renal failure with captopril. 637 20

Radionuclide scintigraphy of the renal transplant has assumed an important role in disclosing the complications that beset this life-prolonging procedure. Renal ischemia, whether caused by mechanical obstruction of the blood vessels or ureter or immunological rejection, can be detected by qualitative and quantitative perfusion studies using 99mTc-complexes such as pertechnetate, glucoheptonate and DTPA. Similarly, parenchymal agents such as radiohippurate and 99mTc-DTPA can be quantitated for uptake and their drainage patterns monitored to reveal possible underlying obstructive uropathy and urine extravasation. The literature is replete with mathematical strategems for quantitating perfusion and parenchymal transit of the tracers, but none are truly specific enough to be diagnostic of a given cause of renal ischemia. Serial quantitative radionuclide studies should be obtained during the first 2-3 wk after transplantation with the view of noting an improvement or deterioration of the quantitation parameters as a guage of progress. A deterioration may anticipate biochemical manifestations by 24-48 hr, but it is not specific and must be interpreted in light of the clinical circumstances or necessitate invasive procedures for a definitive diagnosis.
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PMID:Renal transplant evaluation. 676 Apr 1

Nuclear magnetic resonance (NMR) images obtained after unilateral ligation of the ureter, renal artery, or renal vein in the rat were analyzed and compared with NMR images of the normal rat kidney. Anatomic and functional correlation of the induced renal lesions was made by concurrent CT and by gross examination of the excised kidneys. Many normal anatomic structures at the level of the renal hilum can be identified by high resolution NMR imaging. Differentiation of urine from renal parenchyma permits detection of gross changes both in renal function and in the mass of the renal parenchyma. NMR imaging is capable of diagnosing hydronephrosis, acute renal ischemia, and acute venous congestion in this rat model. In addition, a trend toward prolongation of the relaxation times T1 and T2 for abnormal renal parenchyma is demonstrated.
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PMID:Nuclear magnetic resonance imaging of induced renal lesions. 685 28

Six patients in this series of 543 renal transplants (1.10%) suffered a post-transplant renal segmental infarct of the donor kidney because of occlusion of an accessory renal artery. Five grafted kidneys had multiple renal arteries. Patients presented with symptoms of a caliceal fistula and were treated by partial (25 to 40%) transplant nephrectomy, followed by closure and tissue coverage with either parietal peritoneum (4 patients) or lyophilized human dura mater sealed with fibrin (2). In 2 cases the renal ischemia and necrosis involved the ureter, and a pyelo-pyelostomy was performed. One patient died of cardiorespiratory complications immediately postoperatively. Five years postoperatively all kidneys functioned well without recurrence of fistula and 5 patients returned to a normal life-style. The combination of radical excision and tissue closure, plus ureteral substitution when needed was an effective treatment that prevented loss of the graft.
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PMID:Caliceal fistula formation following renal transplantation: management with partial nephrectomy and ureteral replacement. 786 97

Experiments were conducted in anesthetized cats to determine if spinal neuronal responses to activation of renal receptors are tonically modulated by descending spinal pathways. Eighty-seven thoracolumbar spinal neurons with renal and somatic input were tested for responses to occlusion of the renal vein, renal artery, and ureter before, during, and after cooling the spinal cord rostral to the recording site. Cooling increased the number of neurons that responded as well as the magnitude of the responses to renal vein (RVO), renal artery (RAO), and ureteral occlusion (UO). RVO increased cell activity of 21 neurons from 12.5 +/- 2.7 to 31.7 +/- 6.0 spikes/s during cooling. UO increased cell activity of 24 neurons from 9.0 +/- 2.1 before cooling to 25.0 +/- 4.9 spikes/s during cooling. Cold block increased the magnitude of both types of responses to RAO that were due to mechanical deformation of the renal artery and prolonged renal ischemia. These data show that the majority of spinal neuronal responses to renal receptor stimulation are modulated by tonic inhibitory influences. Thus these results provide a mechanism by which the brain may control spinal circuitry that underlies reflexes of renal origin.
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PMID:Tonic descending modulation of spinal neuronal responses to activation of renal receptors. 828 69


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