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

An in vivo ureteral perfusion technique combined with a recently described methodology was used to study the effects of caffeine on ureteral motility patterns. Effects of the drug on the disused ureteric stump were also noted. The results showed a dose-related inhibition to complete cessation of peristalsis. Proposed mechanisms of caffeine effect on the ureter are discussed.
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PMID:The effect of caffeine on uretheral motility. 90 10

The effects of caffeine on the electrical and mechanical activity of the guinea-pig ureter smooth muscle were studied. Under untreated conditions caffeine mainly showed inhibitory action on the ureter, inhibiting the evoked action potentials and phasic contractions as well as potassium contracture. Caffeine was also found to suppress the low-Na contracture of Na-loaded ureter muscle. It is established that Na-loaded tissue is able to generate transient contracture in response to caffeine application at 37 degrees C. These caffeine contractures could be evoked under completely removed [Ca2+]0 and in the presence of high doses of Ca-channel blockers (nifedipine, diltiazem, Mn ions) and could be reversibly blocked by tetracaine, procaine and benzocaine. Caffeine contractures could also be produced by the ureter muscle placed in isotonic K-solution. Cooling significantly potentiated low-Na, potassium and caffeine contractures of the ureter muscle. Filling of the store is totally dependent on the entry of Ca ions from the extracellular Ca2+ store sites which sequester Ca ions entering the cell on either Na-Ca exchange or via voltage operated Ca channels.
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PMID:Effects of caffeine on the electrical and mechanical activity of guinea-pig ureter smooth muscle. 243 12

1. Ionic currents underlying the action potential were recorded from enzymatically isolated smooth muscle cells of guinea-pig ureter. 2. The action potential recorded from a single cell was similar to that from a multicellular preparation. It showed repetitive spikes on a plateau potential which followed the first spike. Treatment with 10 mM-tetraethylammonium (TEA) increased the amplitude and duration of the plateau phase and abolished the repetitive spikes. 3. Under voltage clamp mode, at least two (maybe three) kinds of outward currents were activated during depolarizing pulses. The main outward current was Ca2+-dependent K+ current (IK(Ca], which was mostly blocked in Ca2+-free solution, or by application of 1 mM-cadmium (Cd2+) or 2 mM-tetraethylammonium (TEA). IK(Ca) was greatly decreased by treatment with 5 mM-caffeine or an addition of 10 mM-EGTA in a pipette solution. 4. In the presence of 1 mM-Cd2+ and 2 mM-TEA, a small transient outward current remained. 4-Aminopyridine (1 mM) suppressed the transient outward current by about 40%. Time- and voltage-dependent delayed rectifier outward currents were small in ureter cells. An inwardly rectifying K+ current was not detected. 5. An application of 1 mM-Cd2+, 5 mM-cobalt (Co2+), 1 mM-lanthanum (La3+) or 0.1 microM-nifedipine completely blocked the action potential. Replacement of 80-90% of extracellular Na+ with Li+ or Tris almost abolished the plateau potential and repetitive spikes but did not change significantly the first spike. 6. In the presence of 30 mM-TEA, the inward current elicited by depolarization was monophasic and lasted for more than 1 s. Application of 1 mM-Cd2+, 1 mM-La3+, 0.1 microM-nifedipine, or 5 mM-Co2+ completely blocked inward current. The replacement (87%) of extracellular Na+ ions with Li+, Tris, sucrose or TEA speeded up the decay of inward current; the inward current decreased by 10-60% at the end of a 500 ms pulse. 7. Even in low-Na+ solution (120 mM-TEA), the inactivation of ICa had a quite slow component (tau = 1 s), in addition to another faster component (tau = 100 ms) at 0 mV. When short depolarizing clamp pulses (50 ms) were repetitively applied at short intervals (50 ms) and with interpulse voltage of -10 or -20 mV to mimic the repetitive spikes on the plateau of the action potential, the decline of peak Ca2+ current during the train of pulses was smaller than the decay of Ca2+ current during a long pulse.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Ionic currents in single smooth muscle cells from the ureter of the guinea-pig. 248 52

We reviewed 49 patients with urothelial tumors of the ureter: 33 male and 16 female patients with a mean age of 64.8 and 66.3 years, respectively. Median followup was 83 months. Gross hematuria was present in 29 patients and a silent kidney was found in 21. The majority of the tumors were in the distal ureter and approximately 50 per cent of the patients had synchronous or asynchronous urothelial tumors. The majority of the patients had low grade, low stage tumors (75 per cent). A total of 21 patients underwent local resection and none died of tumor. Only 1 of these 21 patients had an ipsilateral recurrence. Nephroureterectomy was performed in 24 patients and 5 of them died of ureteral tumor, including 4 in whom periureteral tumor growth initially was recorded. The prognosis of patients with papillomas or grades 1 to 3, stages Pa to P1 ureteral tumors was excellent and a conservative approach is recommended for these patients. Abuse of combination analgesics containing phenacetin, phenazone and caffeine may be a risk factor for development of ureteral tumors.
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PMID:Carcinoma of the ureter: a clinicopathologic study of 49 cases. 248 33

Results from a population-based case-control study of cancer of the renal pelvis and ureter are reported. Telephone interviews were conducted with 187 residents of Los Angeles County diagnosed with cancer of the renal pelvis and ureter over a 4-year period ending December 31, 1982, and with individually sex-, age- and race-matched neighborhood controls. The major risk factor identified for cancer of the renal pelvis and ureter was cigarette smoking. Subjects who smoked more than 25 years had a relative risk of 4.5 of developing these tumors, compared to nonsmokers (P less than 0.0001). Heavy use of over-the-counter analgesics was also associated with a significant increase in risk; it appears that an elevated risk was conveyed by all the major active constituents of those compounds currently marketed in the United States, aspirin, caffeine, and acetaminophen. Persons who had used these drugs for 30 consecutive days at any time in their life preceding diagnosis had twice the risk of developing cancer of the renal pelvis or ureter compared to persons not reporting such use (P less than 0.01). Heavy coffee drinkers (greater than or equal to 7 cups/day) had a 1.8-fold increase in risk compared to nondrinkers. Although risk tended to increase with increasing consumption, this result was not statistically significant. The risk associated with heavy coffee consumption was reduced to 1.3 after adjusting for smoking. Nine cases compared to no controls reported a first degree relative with kidney cancer. A history of kidney stones was associated with an increased risk of cancer of the ureter (relative risk = 2.5) that was not, however, statistically significant.
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PMID:Analgesics, cigarette smoking, and other risk factors for cancer of the renal pelvis and ureter. 291 49

The in vitro guinea pig ureter responds to 5-s trains of electrical stimuli with two contractions: the first, an "on" response, occurs within 0.1-0.3 s after the onset of the stimulus train; the second, an "off" response, occurs 0.2-1.0 s after the termination of the stimulus train. Force decreases between the two responses during a time when the stimulus is still being delivered. Longer duration and/or higher frequencies of stimuli within the train are required to elicit the off response than the on response. Neither the on nor the off response appears to be neurally mediated, since both responses are unchanged by tetrodotoxin, phentolamine, atropine, and pyrilamine. Decreasing temperature from 37 to 22 degrees C decreases the amplitude of the on response and increases the amplitude of the off response. Calcium-free solution, 2 mM ethylenediaminetetraacetic acid (EDTA), 1 mM Mn2+, and 1 microM verapamil abolish the on response at a time at which the off response continues to persist. Conversely, 0.5 mM caffeine and 0.1 mM theophylline abolish the off response, whereas they only slightly reduce the on response. These data suggest that the on response depends on extracellular free calcium, whereas the off response is more dependent on bound or stored calcium.
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PMID:"On" and "off" responses of guinea pig ureter. 391 13

1. The aim of this study was to assess the role of sarcoplasmic reticulum (SR) calcium (Ca2+) in the smooth muscle relaxant and hyperpolarizing actions of calcitonin gene-related peptide (CGRP) in the guinea-pig ureter. 2. CGRP (0.1 microM) rapidly and transiently reduced myogenic phasic contractions (twitches) produced by electrical field stimulation (EFS). Approximately 70% of the response to CGRP was antagonized by glibenclamide (1 microM). 3. Cyclopiazonic acid (CPA, 10 microM), ryanodine (100 microM) and thapsigargin (1 microM) reduced only the glibenclamide-sensitive component of the response to CGRP (0.1 microM) but did not modify the mechano-inhibitory effect of cromakalim (3 microM). A low concentration of CPA (1 microM), assumed to produce a limited impairment of Ca2+ uptake from the stores, prolonged the duration of the inhibitory response to CGRP. Pre-exposure to caffeine (5 mM) inhibited the suppression of twitches by CGRP or cromakalim. 4. When the frequency of EFS was increased, the suppression of twitches by CGRP was reduced. Under these conditions, CPA (1 microM) again prolonged the duration of the inhibitory response to CGRP. 5. CGRP (0.1 microM) and cromakalim (3 microM) markedly depressed the phasic component of contractions to 80 mM KCl. CPA (10 microM) antagonized the inhibitory effect of CGRP but not that of cromakalim. Inhibition of the tonic contraction to 80 mM KCl by CGRP was insensitive to CPA. 6. In sucrose gap experiments, a 5 min exposure to CGRP (0.1 microM) or cromakalim (3 microM) produced a sustained membrane hyperpolarization. Caffeine (5 mM) produced a glibenclamide-sensitive transient hyperpolarization followed by a sustained depolarization. When tested in a Ca(2+)-free medium the hyperpolarization produced by CGRP, cromakalim or caffeine was reduced. In normal Krebs, pre-exposure to CPA (10 microM, 60 min) only abolished the hyperpolarization induced by CGRP. In contrast, 5 min after a caffeine challenge (5 mM) the hyperpolarizations induced by CGRP or cromakalim were reduced. The CGRP-induced hyperpolarization was insensitive to apamin (0.1 microM) or charybdotoxin (0.1 microM). 7. We conclude that the K channel-opening action of CGRP in the guinea-pig ureter requires the mobilization of intracellular Ca2+ from a caffeine- and CPA-sensitive store, leading to transient activation of glibenclamide-sensitive K channels. The K channel-opening action of caffeine appears to involve Ca2+ mobilization from a store which is insensitive to depletion by CPA.
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PMID:Role of intracellular Ca2+ in the K channel opener action of CGRP in the guinea-pig ureter. 883 77

1. We have investigated the internal Ca2+ store and its ability to affect contraction by simultaneously measuring force and Ca2+ in the ureter from guinea-pig and rat. Both species responded in a similar manner to electrical stimulation and depolarization with high-K+, generating plateau-type action potentials and increasing intracellular calcium ([Ca2+]i) and force. 2. In the guinea-pig, carbachol had no effect on [Ca2+]i and force in the resting ureter. In contrast, resting rat ureter always responded with a large [Ca2+]i rise and maintained force to carbachol in Ca(2+)-containing solution, and in Ca(2+)-free solution it showed a transient increase in [Ca2+]i and force. This Ca2+ release and force development was also present in both polarized and high-K(+)-depolarized preparations and was insensitive to nifedipine, suggesting the presence of a receptor-coupled pathway of Ca2+ release in rat ureter. 3. Caffeine was able to produce a release of Ca2+ from the internal store of guinea-pig ureter and elicit contraction. However, rat ureter failed to respond to caffeine. In the presence of La3+, the caffeine response in the guinea-pig ureter and carbachol response in the rat ureter, elicited in Ca(2+)-free solutions, were always increased and prolonged and could be repeatedly evoked, suggesting similarity in Ca2+ uptake behaviour of the store in both species. 4. Ryanodine blocked the caffeine responses of the guinea-pig ureter elicited both in Ca(2+)-containing and Ca(2+)-free solutions, both in the absence and presence of La3+. However, ryanodine failed to prevent the rat ureter responding to carbachol, suggesting that carbachol was releasing Ca2+ from a ryanodine-insensitive channel in the sarcoplasmic reticulum (SR). 5. Cyclopiazonic acid, which inhibits the SR Ca(2+)-ATPase, abolished the effects of both caffeine and carbachol in Ca(2+)-free solutions in guinea-pig and rat, respectively. 6. We conclude that there is a major difference in the mechanisms of Ca2+ release in the internal Ca2+ store of smooth muscle from guinea-pig and rat ureter. The data suggest that the guinea-pig store is purely a calcium-induced calcium release (CICR)-type store and that the rat store is a pure receptor-operated Ca2+ store.
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PMID:Major difference between rat and guinea-pig ureter in the ability of agonists and caffeine to release Ca2+ and influence force. 884 29

Recent work has indicated that there is a major difference in the Ca2+ store of smooth muscle from rat and guinea-pig ureter; with the rat store being agonist-sensitive but ryanodine insensitive and the guinea-pig store being ryanodine sensitive but agonist insensitive [Th. V. Burdyga, M.J. Taggart, S. Wray, J. Physiol. 489 (1995) 327-335]. We have therefore examined directly the mechanism of Ca2+ release from the internal Ca2+ store (SR). Following permeabilisation with alpha-toxin or beta-escin the SR was Ca(2+)-loaded before application of carbachol or caffeine. Only carbachol evoked a transient contraction in rat ureter. The carbachol-induced contraction was blocked by heparin and cyclopiazonic acid (CPA) but not ryanodine. Only caffeine produced contraction in guinea-pig ureter, and this was blocked by ryanodine. Direct application of IP3 caused a small transient contraction in rat but not guinea-pig ureter. We conclude that rat ureter possesses only an IP3 sensitive store while guinea-pig ureter only has a ryanodine sensitive store.
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PMID:The mechanism of Ca2+ release from the SR of permeabilised guinea-pig and rat ureteric smooth muscle. 955 Oct 92

This paper discusses the role of Ca2+-induced Ca2+ release (CICR) and inositol-1,4,5-trisphosphate (InsP3)-induced Ca2+ release (IICR) from the sarcoplasmic reticulum (SR) in the control of contractile activity in the ureter. The Ca2+ store in guinea-pig ureter has been found to be exclusively a CICR type with ryanodine receptors (RyRs) present. In the rat ureter the SR store is exclusively an IICR type with InsP3 receptors (InsP3Rs) present. Guinea-pig ureteric cells in vitro and in situ have been found to generate Ca2+ sparks--small localized, transient releases from RyRs. The sparks are enhanced by caffeine and blocked by emptying the SR. In rat cells Ca2+ puffs occur in response to agonists, representing the opening of InsP3Rs. The puffs can be abolished by heparin or store emptying. These SR Ca2+-release events affect the excitability of the ureteric cells. In guinea-pig cells, spontaneous transient outward currents (STOCs) can be recorded in response to caffeine application (an agonist for RyR), followed by a shortening of the plateau phase of the action potential. This in turn causes a decrease in the amplitude and duration of the contractions of the ureter. If the SR is inhibited then STOCs are abolished, the action potential plateau prolonged and force increased. Thus it is concluded that the SR acts to limit contraction in the guinea-pig ureter. The mechanism underlying this involves its Ca2+ release being directed to Ca2+-activated K+ channels on the surface membrane and causing STOCs and hyperpolarization, and controlling the duration of the action potential. In rat ureter IICR acts to potentiate force via membrane depolarization and increased L-type Ca2+ entry into the cells. Thus the SR can alter cell signalling and excitation-contraction coupling in the ureter, but its precise role is species dependent. The ureter, with its species-dependent expression of either IICR or CICR provides an ideal system (a natural transgenic model) for studying the SR. Eventually, we will be able to apply this knowledge to the human ureter, to increase our understanding of its functioning in health and disease.
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PMID:Sarcoplasmic reticulum function and contractile consequences in ureteric smooth muscles. 1216 10


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