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)

We compared the effect of the renal nerves on renal function, plasma renin activity, and renal renin and angiotensinogen mRNA contents in Wistar rats and spontaneously hypertensive rats (SHR). Rats were anesthetized with sodium pentobarbital, the left kidney was exposed, its nerves were sectioned, the ureter was cannulated, and a flow probe was placed on the renal artery. The renal nerves were stimulated for 1 hour to reduce renal blood flow by 15% and 30%, after which blood was removed for measurement of plasma renin activity, and kidneys were analyzed for renal renin and angiotensinogen mRNA. Frequency-related reductions in filtration rate were similar, from 15% to 50%, as was sodium excretion, from 30% to 70%, in both SHR and Wistar rats. Basal plasma renin activity and responses to nerve stimulation in SHR were approximately half those of Wistar rats (all P < .001). SHR renal renin mRNA concentrations were approximately three quarters those of Wistar rats and were unchanged by either low- or high-level renal nerve stimulation, whereas the higher rate increased renin mRNA approximately threefold (P < .05) in the Wistar rats. SHR renal angiotensinogen mRNA was one quarter that of the Wistar rats and was unaffected by nerve stimulation, whereas in the Wistar rats it was increased threefold (P < .05) by the low but not high level of nerve stimulation. These findings show that whereas the renal nerves are able to modulate hemodynamic and tubular functions relatively normally in SHR, their ability to increase renin release, renal renin, and angiotensinogen mRNA levels is depressed.
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PMID:Renal nerves, renin, and angiotensinogen gene expression in spontaneously hypertensive rats. 772 1

Post-prostatectomy syndrome (PPS) is characterized by hyponatremia after absorption of glycine irrigant. To study the pathogenesis of this syndrome, adult male rats with ligated ureters were infused over 15 minutes with 7.5 ml/100 g body weight of isosmotic glycine (N = 9) or mannitol (N = 9) and were compared to non-infused, ureter-ligated controls (N = 9). Immediately post-infusion, plasma sodium had decreased similarly in glycine- and mannitol-infused animals (111 +/- 2 vs. 106 +/- 1 mmol/liter), but plasma osmolality remained at control levels in both groups (285 +/- 1 vs. 288 +/- 1 mOsm/kg). Two hours post-infusion, hyponatremia was stable in the mannitol group (108 +/- 1 mmol/liter), but in the glycine group plasma sodium increased significantly (to 120 +/- 1 mmol/liter). Plasma osmolality two hours post-infusion was maintained in both the glycine (287 +/- 2) and mannitol (292 +/- 2) groups. Brain water in glycine-infused animals (3.90 +/- 0.01 liter/kg dry wt) was not significantly different from the mannitol-infused group (3.85 +/- 0.01) and only 1.8% higher than non-infused controls (3.83 +/- 0.02). Brain tissue glycine did not differ between the three groups. In contrast, muscle water two hours post-infusion in the glycine group was 6% higher than mannitol-infused and 13% higher than non-infused animals. Muscle glycine content in the glycine group (67 +/- 4 mM/kg dry tissue) was increased when compared to both mannitol-infused (25 +/- 1) and non-infused (20 +/- 1) groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycine-induced hyponatremia in the rat: a model of post-prostatectomy syndrome. 773 Nov 56

Kidney function of the euryhaline toad Bufo viridis was studied in animals acclimated to tap water and solutions of NaCl (230 and 500 mosmol.kg-1 H2O) and urea (500 mmol.l-1) in steady-state conditions. An ureter was catheterized for continuous urine collection and blood was sampled from an iliac artery. A single injection of 3H-inulin served for estimation of glomerular filtration rate: this was in the range of 15-27 ml.kg-1.h-1 and did not differ significantly in any of the acclimation conditions. Urine flow, on the other hand, varied considerably and was highest in tap water (18.2 +/- 3.2 ml.kg-1.h-1; urine/plasma inulin ratio = 0.88), lower in 230 mosmol.kg-1 H2O NaCl solution (13.5 +/- 3.9 ml.kg-1.h-1; u/p inulin ratio = 1.73) and lowest in 500 mosmol.kg-1 H2O NaCl or urea acclimation solutions (5-7 ml.kg-1.h-1; u/p inulin = 3.7-4.2). Clearance of free water was high in the tap water group, lower in 230 mosmol.kg-1 H2O NaCl solution, and much lower in the hyperosmotic acclimation conditions. Clearances of both Na+ and Cl- were similar under our experimental conditions, but changed independently in accordance to the composition of the acclimation solution. Potassium clearance was similar in all acclimation conditions, and a constant plasma K+ concentration was maintained. Urea clearance was high in tap water and 500 mmol.l-1 urea acclimation groups and low in the NaCl acclimations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function at steady state in a toad (Bufo viridis) acclimated in hyperosmotic NaCl and urea solutions. 773 33

NADPH-diaphorase histochemical staining and electrical field stimulation (EFS) were performed in vitro to investigate whether nitric oxide (NO) is involved in non-adrenergic non-cholinergic (NANC) inhibitory neurotransmission of pig intravesical ureter. NADPH-diaphorase activity was expressed in nerve trunks and thin nerve fibres around arteries and muscular bundles in the intravesical ureter. Relaxations to EFS were tetrodotoxin (10(-6) M)-sensitive which indicates their neurogenic origin. Addition of the NO-synthase inhibitor, L-NG-nitroarginine (L-NOARG, 3 x 10(-5) M), abolished the electrically induced relaxations, which were significantly reversed by L-arginine (3 x 10(-3) M). Addition of acidified sodium nitrite (NaNO2, 10(-5)-10(-3) M) evoked concentration-dependent relaxations of ureteral strips which were unaffected by L-NOARG. It is concluded that NO synthase is present in nerve fibres and NO seems to mediate the inhibitory neurotransmission of the porcine intravesical ureter.
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PMID:Nitric oxide is involved in the non-adrenergic, non-cholinergic inhibitory neurotransmission of the pig intravesical ureter. 778 45

The participation of Na+ in regulation of intracellular Ca++ content and in formation of spontaneous action potentials of guinea-pig ureter was studied. It was shown that the fast decrease of intracellular Ca++ in the Ca(++)-loaded muscles was accompanied by enhancement of Na+ content in the cells. The concentration gradient of Na+ was found to define the effectiveness of Ca(++)-extrusion from Ca(++)-loaded cells. The decrease of intracellular Ca++ showed a sigmoidal dependence on Na+ content in the medium. A correlation was established between the concentration gradient of Na+ and the formation of action potential plateau of ureter smooth muscle cells. The duration of action potential plateau decreased in accordance with Ca++ efflux and Na+ influx. The results confirmed the participation of Na(+)-Ca++ exchange mechanism in support of Ca++ cellular homeostasis as well as in the generation of action potentials of guinea-pig ureter.
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PMID:Na(+)-Ca++ exchange mechanism in smooth muscle of the ureter. 779 52

1. Mechanisms involved in the regulation of intracellular pH (pHi) in smooth muscle cells of guinea-pig ureter have been investigated using double-barrelled pH-sensitive microelectrodes in isolated strips of tissue. 2. Removal of CO2-HCO3- from the superfusing solution caused a fall in the steady-state pHi except in a few cells which had been excised from the animal for many hours (usually > 24 h). The pHi value was 7.22 +/- 0.09 (n = 89; mean +/- S.D. of an observation) in solution buffered with 5% CO2-21 mM HCO3-, compared with 6.92 +/- 0.24 (n = 67) in the nominal absence of CO2-HCO3-. Recovery from experimentally induced acidosis was faster in the presence, rather than nominal absence, of CO2-HCO3- (mean half-times of 2.7 +/- 0.7 min, n = 41, and 4.6 +/- 1.3 min, n = 12, respectively). These results suggest the presence of both HCO(3-)-dependent and -independent mechanisms for the effective extrusion of acid equivalents. 3. Recovery from acidosis was dependent on external Na+ (Na+o) in both the presence and nominal absence of CO2-HCO3-, with an apparent half-maximal activation at approximately 4 and 20 mM Na+o, respectively. Removal of Na+o in the steady state caused a fall in pHi which proceeded at a faster rate in the presence rather than in the nominal absence of CO2-HCO3-. 4. Amiloride (100 microM-1 mM) reversibly inhibited the recovery from acidosis and caused a fall in the steady-state pHi when applied in the nominal absence of CO2-HCO3-, but had no measurable effect on either the recovery from acidosis or steady-state pHi in the presence of CO2-HCO3-. These results suggest that Na(+)-H+ exchange was responsible for extrusion of acid equivalents in the nominal absence of CO2 and HCO3-, but that it played little part under more physiological conditions. 5. Although Na(+)-H+ exchange appeared to be activated below a pHi of about 7.2, it was incapable of maintaining a 'normal' pHi in the nominal absence of CO2-HCO3- in freshly excised cells, where values between 6.06 and 6.89 were recorded. Only in aged preparations, in which the intrinsic intracellular acid loading was substantially reduced (as judged from the rate of acidification on application of amiloride in the nominal absence of CO2-HCO3-) did the steady-state value approximate to that observed in the presence of CO2-HCO3-, at about 7.2.
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PMID:Regulation of intracellular pH in the smooth muscle of guinea-pig ureter: Na+ dependence. 779 29

1. Intracellular pH (pHi) of smooth muscle cells in isolated strips of guinea-pig femoral artery was measured using double-barrelled pH-sensitive microelectrodes. 2. In modified Krebs solution equilibrated with 5% CO2, pHi was 7.26 +/- 0.14 (n = 36; mean +/- S.D. of an observation) and the membrane potential (Em) was -60.5 +/- 5.5 mV. Removal of CO2 from the superfusing solution caused an immediate transient alkalosis before pHi stabilized at much the same value (7.28 +/- 0.14; n = 16) as in the presence of CO2. 3. The rate of recovery of pHi from experimentally induced acidosis was not measurably affected by the presence or nominal absence of CO2-HCO3-. 4. Application of amiloride (100 microM) blocked recovery from acidosis in the nominal absence of CO2-HCO3- and caused a progressive fall in pHi. In the presence of CO2-HCO3-, application of amiloride allowed a slow recovery to pHi 6.7-7.0, but completely prevented full recovery to the normal pHi. 5. Removal of extracellular Na+ (Na+o) caused a dramatic, progressive fall in pHi in both the presence and nominal absence of CO2-HCO3-. 6. The amiloride-insensitive extrusion of acid equivalents observed in the presence of CO2-HCO3- to pHi 6.7-7.0 was inhibited by removal of Na+o but was not affected by preequilibration with DIDS (see Methods). 7. It is concluded that Na(+)-H+ exchange is largely responsible for the effective extrusion of acid equivalents in these arterial cells, at least from relatively small perturbations. A DIDS-insensitive, Na(+)- and HCO3(-)-dependent mechanism provides some recovery from acidosis to a relatively low pHi. 8. Comparison with data obtained in exactly the same manner in smooth muscle cells of the guinea-pig ureter indicates that there are significant differences in the regulation of pHi in different smooth muscles.
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PMID:Regulation of intracellular pH in smooth muscle cells of the guinea-pig femoral artery. 779 30

1. Previously we have shown that an intrarenal infusion of moxonidine, an I1-imidazoline receptor agonist, resulted in a natriuresis which was inhibited by intravenous idazoxan, a selective imidazoline receptor antagonist. Therefore we examined the effects of renal function of intracerebroventricular (i.c.v.) administration of moxonidine with or without i.c.v. idazoxan. 2. Seven days after unilateral nephrectomy, Sprague-Dawley rats had i.c.v. cannulae implanted. Three days later the rats were anaesthetized (pentobarbitone), followed by cannulation of the jugular vein (fluid and drug administration), carotid artery (blood pressure) and the ureter (urine collection). 3. After a 45 min stabilization period, the effect of moxonidine was investigated by the i.c.v. administration of either isotonic saline or moxonidine (0.1, 0.3 or 1 nmol in isotonic saline) administered in 5 microliters over 1 min. All doses of moxonidine resulted in an increase in urine flow with a concomitant increase in sodium excretion without affecting blood pressure. The highest dose of moxonidine (1 nmol) also increased free water clearance. 4. In a second series of experiments, the effects of idazoxan on the natriuretic response to i.c.v. moxonidine were determined. Moxonidine (0.3 nmol) again increased sodium and water excretion as compared to the i.c.v. saline control animals. Pretreatment with i.c.v. idazoxan (0.3 nmol), at a dose which alone failed to alter sodium and water excretion, completely attenuated the renal response to moxonidine. These results are consistent with central I1-imidazoline receptors mediating a moxonidine-induced increase in sodium and water excretion at doses that do not alter blood pressure.
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PMID:Sodium excretion following central administration of an I1 imidazoline receptor agonist, moxonidine. 795 68

We injected 0.3 ml. of polytetrafluoroethylene paste (Polytef) behind the left submucosal ureter in 4 mini-pigs and 4 dogs, and 2 dogs and 2 mini-pigs underwent sham operation and acted as controls. Two mini-pigs were injected with 0.5 ml. polytetrafluoroethylene (Teflon) suspended in 50 ml. of normal saline into a peripheral vein and 2 dogs were injected with 0.5 ml. polytetrafluoroethylene into a bladder vein. In addition, 4 dogs were injected with 0.1 ml. polytetrafluoroethylene paste suspended in 20 ml. saline into the right carotid artery. The lungs and brain from half of the animals who had subureteral and intravascular injection of polytetrafluoroethylene paste as well as sham operated animals were dissolved in sodium hypochlorite solution. The resulting organ suspensions were then centrifuged and the smear preparations of the precipitate were examined by polarized light microscopy, scanning electron microscopy and x-ray microanalysis. Polytetrafluoroethylene paste suspended in saline acted as positive control for polytetrafluoroethylene particles. Lungs and brain from the remaining animals were fixed in formalin solution. The brain and lungs of animals who underwent subureteral injection with a minimal amount of polytetrafluoroethylene paste carefully placed in the submucosal plane showed no evidence of polytetrafluoroethylene on histological examination, polarized light microscopy, scanning electron microscopy and x-ray microanalysis.
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PMID:Particles found in lung and brain following subureteral injection of polytetrafluoroethylene paste are not teflon particles. 802 87

Injection of polytetrafluoroethylene (Teflon) or collagen has been used in the endoscopic treatment of vesicoureteral reflux. Although the principle of an endoscopic treatment is valid, there are concerns regarding the long-term safety and effectiveness of these substances. In search of a different injectable material we conducted experiments using chondrocytes in a biodegradable polymer solution for the treatment of vesicoureteral reflux in an animal model. Reflux was created in 4 mini-pigs and confirmed with a cystogram. Cartilage was obtained from the auricular surface of each animal. Chondrocytes were harvested and expanded in vitro. The cells were individually quantitated and concentrated to 40 million cells per cc. The cell suspensions were mixed with a sodium alginate and calcium sulfate solution. Each pig was injected unilaterally in the subureteral region with the autologous chondrocyte suspension. The opposite ureter served as an internal control in all animals. Cystograms showed resolution of reflux in the treated side and persistence of reflux in the opposite untreated side in each instance. Excretory urograms revealed no evidence of obstruction. Histological examination of the subureteral region demonstrated cartilage. Autologous chondrocytes can be readily harvested, expanded in vitro and injected cystoscopically. The cells survive and form a cartilage nidus that is nonantigenic. This system is able to correct reflux without any evidence of obstruction.
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PMID:Endoscopic treatment of vesicoureteral reflux with a chondrocyte-alginate suspension. 802 88


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