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)

The concentration of major urinary solutes was studied in ureteral urine collected at 15- to 30-s intervals at the onset of acute diuresis induced in anesthetized dogs either by high-ceiling diuretics (mainly ethacrynic acid) or by osmotic diuretics. Phosphate/inulin clearance ratios remained unchanged; potassium/inulin clearance ratios rose rapidly. Principal attention is given to the mechanisms underlying a transient rise in urinary sodium and chloride concentrations during the onset of diuresis. When the data are corrected for washout artifacts from the pelvis and ureter, it can be shown that the initial collection periods are associated with a transient increase in free-water production and by the simultaneous secretion of urea from the interstitium into the tubular fluid. The former coincides in time with the rise in urinary chloride concentration and represents an augmentation of water reabsorbed in the collecting duct, which is relatively impermeable to chloride. Both responses are quantitatively consistent with the transition from a hyperosmotic to isosmotic medullary interstitium.
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PMID:Electrolyte excretion and free-water production during onset of acute diuresis. 113 May 34

By ligation of the ureter, causing partial ureteral stenosis, unilateral hydronephrosis was induced in 10 dogs. Renal function studies including creatine clearance and osmolality determination were performed both before and after the ureteral ligation. The renal function analysis after induction of hydronephrosis included pyelovenous and pyelolymphatic reflux studies, with deposition of dextran in the renal pelvis at different intrapelvic pressures. Analysis with respect to sodium, potassium, chloride and dextran in the thoracic duct lymph, peripheral blood and urine from the intact kidney were performed. The results show a reduction of the renal function in hydronephrosis, little transport of dextran via the lymph and blood, and no significant increase in the lymphatic transport of the studied ions on elevation of the intrapelvic pressure.
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PMID:Renal function in experimental chronic hydronephrosis. I. Backflow studies with dextran. 120 83

In Sodium-deficient solutions both the electrical and mechanical activity of the ureter are reduced. The plateau component of the action potential in the smooth muscle cell of the guinea pig ureter is more affected than the oscillations. Tetrodotoxin, which blocks the action potential in nerves, does not influence activity or conduction in the ureter. This is an important argument for the myogenic conduction of activity in this tissue.
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PMID:The influence of sodium on the electrical and mechanical activity of the ureter. 120 91

The arterial vasodilator activity of endothelium-derived relaxing factor (EDRF) is mediated by activation of the soluble form of guanylate cyclase, causing increased levels of guanosine-3',5'-cyclic monophosphate (cGMP). Because of its extreme lability, the actions of EDRF are local. The ability to monitor changes in renal interstitial fluid cGMP would be of great advantage in clarification of local mechanisms controlling renal function. Utilizing a renal interstitial microdialysis technique, we investigated changes in renal interstitial and urinary cGMP in response to right intrarenal arterial administration of the EDRF inhibitor, NG-monomethyl-L-arginine (L-NMMA), in anesthetized dogs (n = 5) in metabolic balance at a sodium intake of 40 mEq/day. Urine was collected directly from the right and left ureter. L-NMMA at 20-60 micrograms/kg/min significantly decreased right renal interstitial and right urinary cGMP levels (p < 0.01) without changing left renal interstitial and urinary cGMP levels (p < 0.01). L-NMMA at 100 micrograms/kg/min decreased both right and left renal interstitial and urinary cGMP levels (p < 0.01). These data demonstrate the ability to monitor renal interstitial cGMP in vivo. There was a dose-dependent decrease in renal interstitial and urinary cGMP in response to intrarenal EDRF inhibition. Additionally, they suggest that EDRF acts as a renal paracrine substance through the modulation of renal interstitial cGMP.
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PMID:Endothelium-derived relaxing factor modulates renal interstitial cyclic GMP. 128 58

Previous in vitro experiments demonstrated the reduced microhardness of calcium oxalate monohydrate (COM) calculi, relative to dry values, when saturated with an alkaline solution (pH = 9.5). Nineteen patients with a COM calculus in the distal ureter which had been resistant to prior extracorporeal shock wave lithotripsy in situ, were treated when the stone was surrounded by alkaline urine. The urine of 14 patients was alkalinized orally by administration of acetazolamine and citrate solution; in 5 other patients direct percutaneous irrigation of sodium bicarbonate via a nephrostomy tube was carried out. The urinary pH just before lithotripsy was greater than or equal to 9 in 17/19 patients. 4,000 shock waves, averaging 18.1 kV generated by the Siemens Lithostar, were delivered onto the calculus. No significant increase of comminution rate was apparent at radiographic control immediately after the treatment and only in half of the cases was evacuation obtained within 3 months.
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PMID:Effect of alkalinization on calcium oxalate monohydrate calculi during extracorporeal shock wave lithotripsy: in vivo experiments. 131 63

Preliminary studies determined that, unlike other purported alpha-2 adrenoceptor agonists, 2,6-dimethyl clonidine (2,6-DMC) increased urine flow rate independent of vasopressin. We therefore compared the dose-response curves of three alpha-2 adrenoceptor agonists, clonidine, UK 14,304 and 2,6-DMC. Unilaterally nephrectomized Sprague-Dawley rats were anesthetized and the left kidney was exposed and the ureter cannulated. A 31-gauge needle was advanced into the renal artery to permit direct intrarenal infusion of the study drugs. All three agonists produced a dose-related increase in urine flow rate and sodium excretion. A clear opposite rank order of potency was observed when the urine flow rate was analyzed as free water and osmolar clearance. For free water clearance, clonidine much greater than UK 14,304 much greater than 2,6-DMC, with 2,6-DMC producing little change. The effect on osmolar clearance was opposite with 2,6-DMC much greater than clonidine = UK 14,304. The V2 antagonist [1-(beta-mercapto-beta,beta-pentamethylene-proprionic acid), 2-d-isoleucine,4-isoleucine]arginine-vasopressin blocked the effects of clonidine but not 2,6-DMC. In a water-loaded rat model, 2,6-DMC but not clonidine increased the delivery of filtrate out of the proximal segments of the nephron. These results are consistent with the postulate that lower doses of 2,6-DMC increase solute excretion independent of vasopressin, possibly in proximal segments of the nephron. Clonidine on the other hand increases free water clearance and this effect is mediated through an interaction with the renal actions of vasopressin. Whether these disparate effects represent two distinct receptors or two sites of alpha-2 adrenoceptors in the kidney is not known.
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PMID:Opposite rank order of potency for alpha-2 adrenoceptor agonists on water and solute excretion in the rat: two sites and/or receptors? 135 Oct 96

A partial obstruction of the left ureter was created in weanling (3-week-old) rats. Renal function was studied after 7-9 weeks and compared to that in age-matched controls. Arterial blood pressure was found substantially increased. During normal hydration, the hydronephrotic kidney had low excretions of urine, potassium, osmoles and, especially, sodium. The contralateral, intact side showed no compensatory traits. On volume expansion, the hydronephrotic kidney demonstrated an unimpaired reacting capacity, leading to normalization of urine, sodium and osmole excretions and even to supernormal renal blood flow, glomerular filtration and potassium excretion. On the intact side, the excretion of potassium was increased like that on the hydronephrotic one, while excretions of urine, sodium and osmoles were increased even more. The fact that the intact kidney handled most of the urine excretion was interpreted as the result of a mechanism protecting the obstructed kidney from additional pressure insults while homeostasis was maintained. The arterial hypertension may result from the combination of retention of fluid and sodium by the hydronephrotic kidney and the absence of compensation by the intact kidney during normal hydration--like that in everyday life. The functional changes during normal hydration were generally more severe than those we found after obstruction in neonatal and adult rats, in which arterial hypertension was never observed. The clinical implication would be that the kidney may be less tolerant to pressure rises during the infant year. Changes due to obstruction are known to occur rapidly, but after that neither progress nor reverse.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Partial ureteric obstruction in weanling rats. II. Long-term effects on renal function and arterial blood pressure. 141 99

The effect of sodium vanadate on action potential and twitch contraction of guinea pig ureter was studied and compared with that of ouabain, elevated K+, low temperature, and a Ca agonist (BAY K 8644), which can be expected to exert certain comparative effects. Sodium vanadate markedly potentiated twitch contraction. Potentiation by vanadate was associated with marked prolongation of relaxation time. Sodium vanadate caused only slight depolarization of the membrane but marked changes in action potential. The duration of action potential was prolonged and the number of oscillatory spike potentials increased. These effects were different from those of other treatments. It is concluded that prolongation of action potential and the increase in the number of spikes are the main cause of potentiation of twitch contraction by sodium vanadate. In addition, inhibition of Ca pump activity of the smooth muscle membrane system by vanadate might also be involved in potentiation of twitch contraction.
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PMID:Potentiation of twitch contraction in guinea pig ureter by sodium vanadate. 144 5

The functional morphology of the neuroendocrine system producing sodium influx-stimulating (SIS) peptide in the pond snail, Lymnaea stagnalis, was studied by in situ hybridization and immunocytochemistry. The SIS-peptide, which is 76 amino acids long, stimulates sodium uptake from the ambient medium. Two synthetic DNA probes were used for in situ hybridization. The nucleotide sequences were chosen from the cDNA structure; they encode amino acids 8-17 and 64-73, respectively. SIS-peptide sequences 10-20 and 67-76 were synthesized and antibodies were raised to them and affinity-purified. In addition to these antibodies, a monoclonal antibody raised to a bioactive, high-pressure liquid chromatography (HPLC)-purified brain extract was used for immunocytochemistry. Paraffin sections of central nervous systems and of whole snails were studied. The SIS-peptide system could be identified as the previously described yellow cell (YC) system by comparing alternate sections treated with the DNA probes, stained with the antibodies, or stained with alcian blue-alcian yellow. SIS-peptide neurons (approximately 45) occur in the ganglia of the visceral ring and in the proximal parts of visceral nerves. Axons run in the nerves of these and in several nerves of other ganglia. Numerous axon branches penetrate the perineurium forming a vast central neurohemal area. The SIS-peptide system innervates the pericardium, the nephridial gland, the reno-pericardial canal, the ureter, the spermoviduct and gonadal acini, the anterior aorta, the ventral buccal artery, and the penis protractor muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional morphology of the neuroendocrine sodium influx-stimulating peptide system of the pond snail, Lymnaea stagnalis, studied by in situ hybridization and immunocytochemistry. 162 12

1. Inward currents elicited by depolarization from holding potentials of -80 to -10 mV in single smooth muscle cells isolated from stomach fundus of the rat and ureter of the guinea-pig had two components. The initial fast component (Ifi) was activated and mostly inactivated within 1-2 and 10 ms, respectively, at 21 degrees C. The following sustained component (Isi) lasted over 50 and 500 ms in fundus and ureter cells, respectively. Ifi was blocked by tetrodotoxin but not affected by 0.5 microM-mu-conotoxin in both types of cells. Isi was abolished by the substitution of extracellular Ca2+ with Mn2+. 2. The sensitivity of Ifis to TTX was markedly different in fundus and ureter cells. The half-inhibition was obtained at 870 and 11 nM, respectively. The amplitude of Ifi was highly dependent on extracellular Na+ concentration in a solution containing 2.2 mM-Mn2+ and 0 mM-Ca2+ in both cells. It is concluded that Ifis in these cells are TTX-sensitive and mu-conotoxin-insensitive Na+ currents. 3. Some of the kinetics of INa measured at 10 degrees C were markedly different in fundus and ureter cells. The current-voltage relationships for Ifi in fundus and ureter cells had peaks at about -10 and 0 mV, respectively. The voltage dependence of the steady-state inactivation of Ifi was also significantly different in these cell types. The half-inactivation voltages were about -74 and -45 mV, respectively. The recovery time course from inactivation in fundus cells was about 10 times slower than that in ureter at -80 mV, where it was 25 ms. 4. The contribution of Ifi to the rising phase of an action potential was examined using TTX under current clamp mode at 21 degrees C. A fast notch-like potential elicited by a subthreshold stimulus for action potential generation was blocked by TTX in both types of cells. Action potentials elicited by a stimulus around threshold were occasionally suppressed by TTX, whereas an action potential was never observed when extracellular Ca2+ was replaced with Mn2+. 5. In conclusion, the existence of at least two types of Na+ channel currents, which were distinguished by their TTX sensitivity and kinetics, was strongly suggested in smooth muscle cells from the rat fundus and the guinea-pig ureter. INa in these cells may have a physiological role to accelerate the generation of an action potential by triggering a rapid activation of ICa, while not being essential for activation of action potentials.
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PMID:Sodium currents in smooth muscle cells freshly isolated from stomach fundus of the rat and ureter of the guinea-pig. 166 61


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