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

A 20-year-old woman had 18 hours of pain and anuria associated with a calcium oxalate stone impacted in the distal left ureter. The stone passed spontaneously and the urine output returned. There was no abnormality of the right kidney on excretory urography. We believe that this is a cause of reflex anuria not previously described. Severe pain may be the initiating event in this unusual but interesting syndrome and mechanisms proposed by previous authors are reviewed.
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PMID:Reflex anuria from unilateral ureteral obstruction. 735 36

The prevalence of kidney stones has steadily risen during this century; passage of a calculus and a positive family history increase the probability of recurrence. Findings from recent studies on the cause of renal calculi have stressed crystallization and crystal aggregation of stone minerals from supersaturated urine, rather than excessive organic matrix. Absence of normal urine inhibitors of calcium salts is also stressed. Formation of calcium oxalate stones is the major problem. Therapy with decreased calcium and oxalate intake, thiazides, phosphate salts and allopurinol in various combinations has substantially decreased the prevalence of recurrent stones. The rationale for the use of allopurinol is that uric acid salts enhance the tendency for calcium oxalate to crystallize from supersaturated urine. The hypercalciuria seen in 30 percent to 40 percent of patients with oxalate stones is usually caused by intestinal hyperabsorption of calcium. Although patients with uric acid calculi constitute only a small fraction of those in whom stones form, they represent a group in whom good medical therapy, based on sound physiologic principles, has proved extremely successful. Renal tubular syndromes lead to nephrocalcinosis and lithiasis through hypercalciuria, alkaline urine and hypocitraturia, the latter an inhibitor of calcium salt precipitation. Recent advances in surgical techniques are discussed, including the rationale for removing staghorn calculi. The ileal ureter and coagulum pyelolithotomy deserve special emphasis.
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PMID:Kidney stones. 738 35

Disturbances of carbohydrate metabolism during acute uraemia are characterized by the degradation of liver and muscle glycogen with a simultaneous activation of hepatic gluconeogenesis. After binephrectomy, the substitution of essential amino acids and keto analogues stimulate liver, but not skeletal muscle glycogen synthesis. Serine proves to be an optimal substrate for liver gluconeogenesis and muscle glycogen generation under acute uraemic conditions. Propranolol does not influence glycogenolysis of skeletal muscle in acutely uraemic rats. During starvation, acute uraemia leads to an increase of total carbohydrate content as well as of glycogen and glucose concentrations in heart muscle Alterations in carbohydrate contents are not observed in the kidney after ureter ligation. Enhanced glycogenolysis of skeletal muscle and liver during acute uraemia may be due to activation of phosphorylase kinase caused by the increased serum concentrations of various hormones (glucagon, catecholamines, parathormone) as well as free proteolytic activity, an increase of intracellular Ca2+-concentration and finally by alterations in the structure of contractile proteins.
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PMID:Carbohydrate metabolism and uraemia-mechanisms for glycogenolysis and gluconeogenesis. 745 93

The effect of calcium antagonists nifedipine and verapamil on spontaneous rhythmic contractions of human isolated ureter obtained from donor subjects undergoing kidney transplantation was investigated in comparison with a nonsteroidal antiinflammatory drug indomethacin. Stop-times i.e. the time elapsing from application, were determined for each drug. The rank order of potency at 10(-8) and 10(-7) M concentrations of the drugs was: nifedipine > verapamil > or = indomethacin. However, no significant difference of the stop-times was observed at 10(-6) M concentration of the drugs tested. The rhythmic contractions were re-activated by PGF2 alpha after stoppage with indomethacin but not with nifedipine or verapamil. These results suggest that not only endogenous PG synthesis but also an influx of calcium from the extracellular space is responsible for the spontaneous rhythmic activity of human ureter. The beneficial effects of using calcium antagonists in the treatment of ureteric colic is discussed.
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PMID:The effect of nifedipine and verapamil on rhythmic contractions of human isolated ureter. 750 79

We have investigated the effect of the dihydropyridine calcium channel agonist, Bay K 8644, and of the plant alkaloid blocker of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum, ryanodine, on the refractory period, action potential and mechanical response of the guinea-pig isolated ureter to electrical stimulation. All experiments were performed in ureters pre-exposed to 10 microM capsaicin to eliminate the inhibitory influence exerted by local release of sensory neuropeptides on ureteral excitability and contraction. In organ bath experiments, electrical field stimulation with parameters which produce direct excitation of ureteral smooth muscle (train of pulses at 10 Hz, 5 ms pulse width, 60 V for 1 s) produced tetrodotoxin- (1 microM) resistant phasic contractions. The response to EFS was abolished by nifedipine (1 nM-3 microM) and was enhanced by Bay K 8644 (1 nM-3 microM). In the presence of Bay K 8644 (1 microM), nifedipine (30 microM) abolished the evoked contractions. Ryanodine (10-100 microM) had no significant effect on the amplitude of evoked contraction. The response of the guinea-pig ureter to direct electrical stimulation of smooth muscle is characterized by a refractory period: at least 40 s interstimulus interval was required to produce a second response in all preparations tested. Bay K 8644 (1 microM) markedly reduced the refractory period of the ureter and a similar effect was observed with ryanodine (100 microM). To further analyze the effect of Bay K 8644 and ryanodine on the refractory period, the response of the ureter was investigated over a 10 s period of stimulation (other parameters as above). In control ureters, continuous stimulation for 10 s produced only one phasic contraction just after the beginning of the train of stimuli. In the presence of Bay K 8644 or ryanodine, more than one phasic contraction developed during a 10 s stimulation, i.e. the refractory period became shorter than the train duration. When both Bay K 8644 and ryanodine were tested on the same preparations, an additive excitatory effect was observed on the mechanical response to electrical stimulation. A slight elevation of KCl concentration (5-10 mM) reduced the refractory period of the ureter as observed with ryanodine or Bay K 8644. Application of KCl (80 mM) produced a biphasic contractile response of the ureter: a series of phasic contractions occurred first, which were then replaced by a slowly developing tonic response. Bay K 8644 (1 microM) enhanced both components of the response to KCl. Ryanodine (10 and 100 microM) markedly prolonged the duration of phasic contractions evoked by KCl and, at 100 microM, slightly (about 25%) reduced the amplitude of tonic contraction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of Bay K 8644 and ryanodine on the refractory period, action potential and mechanical response of the guinea-pig ureter to electrical stimulation. 752 May 36

1. We have investigated the effect of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase inhibitor, cyclopiazonic acid (CPA), on electromechanical coupling in the guinea-pig ureter. All experiments were performed in capsaicin-pretreated (10 microM for 15 min) ureters to prevent the release of sensory neuropeptides from afferent nerves. 2. In organ bath experiments, electrical field stimulation (EFS, 10 Hz for 1 s, 5 ms pulse width, 60 V) produced tetrodotoxin- (1 microM) resistant phasic contractions which were enhanced by Bay K 8644 (1 microM) and abolished by nifedipine (10-30 microM). 3. CPA (10 microM) enhanced the EFS-evoked contractions both in the absence and presence of Bay K 8644. The effect of CPA was concentration-dependent between 1 and 30 microM. The response to 10 microM CPA was biphasic: the maximal enhancement (58 +/- 3% increase) was observed within 10-20 min from CPA administration, followed by a decline to a new steady state (25 +/- 5% increase over baseline) at 50-60 min. The effect of CPA was reversed by washout. 4. Ryanodine (100 microM) produced a prompt enhancement of the EFS-evoked contractions of the guinea-pig ureter, which peaked at 42 +/- 3% increase over baseline; the co-administration of CPA (10 microM) and ryanodine (100 microM) produced a peak effect (60 +/- 8% enhancement) which was not different from that produced by CPA alone. With either ryanodine alone or ryanodine plus CPA, the enhancement of the EFS-induced contractions was biphasic, showing a time-course similar to that observed with CPA alone. Tetraethylammonium (10 mM) produced a significantly larger effect (93 +/- 13% increase over baseline) and its effect was sustained throughout the 60 min observation period. 5. In the presence of Bay K 8644, superfusion for 30 min with a low Na+ medium (60% of extracellular Na+ replaced by Li+ or choline) reduced the amplitude of EFS-evoked contractions by 20-35%. In both Li(+)- and choline-substituted media, spontaneous activity developed during superfusion with low Na+ Krebs solution which was suppressed by 10 microM nifedipine. CPA (10 microM) produced a marked enhancement of the EFS-evoked contractions in low-Na+ medium (both Li(+)- and choline-substituted) and this effect was sustained throughout the 60 min observation period. 6. In the absence of Bay K 8644, the response of the ureter smooth muscle to EFS is characterized by a refractory period: an interval of about 30 s was required between two applied stimuli to produce a second response comparable in size to that elicited by the first stimulus. CPA (10 micro M, 10-20 min before)markedly reduced the refractory period of the guinea-pig ureter to EFS.7. CPA (10 micro M, 30-60 min before) increased the phasic component of contraction produced by 80 m MKCl. The tonic component of the response to KCl was slightly but not significantly reduced by CPA,and a 'hump' in the tonic contraction was observed at 1-2 min from addition of KCl.8. In sucrose gap experiments, 10 micro M CPA produced a sustained depolarization of the membrane and reduced the latency between application of electrical stimuli and onset of the action potential; these effects were maintained throughout the 60 min superfusion with CPA. CPA also transiently prolonged the plateau phase of the action potential and increased the peak amplitude of contraction: these effects peaked at about 10-20 min from start of superfusion with CPA and then declined. At the peak of its enhancing effect on contraction amplitude, CPA prolonged the contractile phase of the contraction relaxation cycle.9.Superfusion with a low-Na, choline-substituted Krebs solution produced a reversible membrane depolarization. In the presence of Bay K 8644 (1 micro M), action potentials and phasic contractions were superimposed on this depolarization which were abolished by nifedipine (1O micro M).10. These findings indicate that CPA augments the excitability and affects the contraction-relaxation cycle of the smooth muscle of the guinea-pig ureter, implying a role for sarcoplasmic reticulum Ca2+-ATPase in the regulation of electromechanical coupling. The effects of CPA resemble those produced by ryanodine and the effect of the two agents on the amplitude of contractions is non-additive.It appears that following blockade of the CPA-sensitive SR Ca2+ pump, other mechanism(s) may come into action to reduce intracellular Ca2+. The Na+/Ca2+ exchanger could be involved in the compensatory changes responsible for the fading of the response to CPA.
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PMID:Effect of the Ca(2+)-ATPase inhibitor, cyclopiazonic acid, on electromechanical coupling in the guinea-pig ureter. 753 95

1. Previous studies have established a marked difference in sensitivity to organic calcium channel blockers of the phasic compared with tonic component of the contraction to potassium chloride (KCl) in the guinea-pig ureter. The mechanisms responsible for this difference have remained unsettled. In particular, the possible involvement of non-L-type calcium channels in contractility of the ureter has not been determined. In this study we have re-addressed this problem and, to eliminate any possible contribution of sensory neuropeptides released by KCl from peripheral endings of afferent nerves, all experiments were performed in ureters pre-exposed to the sensory neurone blocking agent, capsaicin (10 microM for 15 min). 2. Increasing concentrations of KCl (10-160 mM) produced phasic and tonic contractions of the guinea-pig isolated ureter: the L-type calcium channel agonist, Bay K 8644 (1 microM), enhanced both components of the contraction to KCl. 3. Nifedipine (1 microM) abolished all responses to increasing concentrations of KCl after 60 min contact time; after a shorter incubation period (15 min), the phasic contractions to low KCl concentrations were still observed, while the tonic responses were abolished. 4. The effects of nifedipine (0.1 nM-1 microM) on the phasic and tonic components of the response to 80 nM KCl were assessed after 15-120 min contact time. Nifedipine was equipotent in inhibiting the tonic response at all times tested, while a marked time-dependency of inhibition toward phasic responses was observed. After 15 min contact time, nifedipine was 181 times more potent in inhibiting tonic than phasic response to KCl, while after 120 min contact time the difference between EC50 values was only 5.4 times. 5. Cadmium chloride (3-30 microM) was equi-effective in inhibiting the phasic and tonic responses to KCl while nickel chloride was ineffective at 10-fold higher concentrations. omega-Conotoxin (0.1 microM) and tetrodotoxin (0.3 microM) were ineffective. 6. The present findings indicate that L-type voltage-dependent calcium channels mediate both phasic and tonic components of the response of the guinea-pig ureter to KCl while neither T-type nor N-type voltage-dependent calcium channels are involved. The marked time-dependency of inhibitory action of nifedipine suggests that L-type voltage-dependent calcium channels which are responsible for the generation of phasic contraction of the ureter are in a low affinity state for interaction with nifedipine.
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PMID:A pharmacological analysis of calcium channels involved in phasic and tonic responses of the guinea-pig ureter to high potassium. 753 37

The properties of the Malpighian tubules of Drosophila melanogaster change along their length. The upstream main segments secrete K(+)-rich fluid at a high rate. From this, the lower tubules reabsorb significant amounts of water and K+. Under stimulation, K+ reabsorption is accelerated. In addition, the lower tubules acidify the fluid passed to them by the main segments and secrete Ca2+ into it, adding to that transported there by the upstream epithelium. In contrast to the lumen-positive transepithelial potential difference (TEP) of the main segments, the TEP in the lower tubules is much lower and becomes lumen-negative close to their downstream junction with the common ureter. We suggest that the role of the lower tubule is to reduce the flow of K(+)-rich fluid that passes to the hindgut; this allows the hindgut to process the flow of excretory fluid more thoroughly.
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PMID:Fluid reabsorption and ion transport by the lower Malpighian tubules of adult female Drosophila. 763 42

1. The effects of noradrenaline (NA) on action potential shape and underlying membrane currents were examined in single smooth muscle cells freshly isolated from the ureter of the guinea-pig. 2. The voltage-dependent Ca2+ current (ICa) elicited upon depolarization from -50 to 0 mV was reduced by 27% upon application of 10 microM NA. This reduction was inhibited or converted to potentiation by internal application of low molecular weight heparin or 5 mM EGTA, indicating that it may be mediated by Ca(2+)-dependent Ca2+ channel inactivation via inositol 1,4,5-trisphosphate production and subsequent Ca2+ release from intracellular Ca2+ storage sites. 3. In contrast, Ba2+ current (IBa) through Ca2+ channels was potentiated by 36% in the presence of 10 microM NA. Internal application of GTP gamma S made it difficult to remove potentiation of IBa by wash-out; internal application of GDP beta S abolished potentiation. 4. NA caused a greater reduction in the transient Ca(2+)-dependent K+ current (IK(Ca)) upon depolarization than it did in ICa. This reduction was inhibited by internally applied heparin, suggesting that the amount of releasable Ca2+ in the storage sites was markedly reduced in the presence of NA. The sustained component of IK(Ca) which gradually increased during depolarization was also reduced by NA. 5. Action potential duration, which was recorded in a standard solution containing Ca2+, was prolonged by the application of NA. 6. It can be concluded that Ca2+ channel activity in ureter smooth muscle cells is regulated by a dual mechanism: Ca(2+)-dependent inhibition and GTP-binding protein-mediated potentiation. Under physiological conditions, both ICa and IK(Ca) were reduced by NA but the reduction of IK(Ca) was much larger than that of ICa; this results in an increase in net inward current during the action potential plateau and prolongs the action potential.
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PMID:Effects of noradrenaline on membrane currents and action potential shape in smooth muscle cells from guinea-pig ureter. 770 30

Two hundred and twenty ureteric stones in 214 patients were fragmented intracorporeally by pneumatic lithotripsy under general/regional anaesthesia in a day care set-up. Patients were followed-up weekly and retreatment was done at 4 weeks where necessary. Majority (77%) of patients were in the age group 21-40 years with a male to female ratio of 2:1. Stone location was 86% in the lower third, 11% in the middle and 3% in the upper third ureter. Size of stones was less than 6 mm in 14%, 7-12 mm in 67% and more than 20 mm in 4% cases. All 81% stones of < 12 mm were fragmented in one treatment session while single treatment rate for stones 13-18 mm was 85% and 44% for more than 20 mm size. Overall non-fragmentation rate was 0.9%. Stone free state at four weeks was 95%. Complications were observed in 8.6% cases which included urosepsis, haematuria and perforations. Infrared spectroscopy (IR) in 45 stones showed majority (64%) to be composed of calcium oxalate. Our experience shows that PL is a safe and effective means of performing intracorporeal lithotripsy for both large and hard ureteric stones.
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PMID:Pneumatic lithotripsy: a new modality for treatment of ureteric stones. 773 Oct 87


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