UMLS:C0403608 - FACTA Search

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

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

The presence of calcitonin-gene related peptide (CGRP)-like immunoreactivity (-LI) in sensory neurons was established by immunohistochemistry and radioimmunoassay (RIA) in combination with high performance liquid chromatography (HPLC). CGRP-immunoreactive (-IR) nerve fibres were present in many peripheral organs including heart, ureter, uterus and gall bladder of guinea-pig and man. The distribution of CGRP-IR nerves in the dorsal horn of the spinal cord, of positive cell bodies in thoracic spinal and nodose ganglia and nerves in peripheral organs was closely related to that of substance P-LI. Double staining experiments revealed that in most cases peripheral CGRP-IR nerve terminals also contained SP-LI. However, different localization of SP- and CGRP-IR neurons was observed in the nucleus of the solitary tract as well as in the ventral horn of the spinal cord. In the heart, CGRP-IR nerves were associated with myocardial cells (mainly atria), coronary vessels, local parasympathetic ganglia as well as with the epi- and endocardia. Three to 4-fold higher levels of native CGRP-LI were observed in the atria than in the ventricles of the heart. HPLC analysis revealed that the major peak of CGRP-LI in the heart of rat and man had the same retention times as the synthetic equivalents. Systemic capsaicin pretreatment and adult guinea-pigs caused a loss of CGRP-IR terminals in the dorsal horn of the spinal cord as well as in peripheral organs including the heart. After capsaicin treatment, the content of CGRP-IR was reduced by 70% in the heart and by 60% in the dorsal part of the spinal cord. In superfusion experiments with slices from the rat spinal cord, a release of CGRP-LI was induced by 60 mM K+ and 3 microM capsaicin in a calcium-dependent manner.
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PMID:Calcitonin gene-related peptide (CGRP) in capsaicin-sensitive substance P-immunoreactive sensory neurons in animals and man: distribution and release by capsaicin. 243 68

The effects of Na-free medium, Na-K pump inhibitors, ATP and Ca++ ion antagonists in calcium channels (verapamil, Mn++) on the slow-wave spontaneous activity of the ureter pace-maker zone were studied under conditions of i. a. perfusion of kidney. A reduction of membrane potential oscillations was observed.
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PMID:[Interaction of ionic membrane mechanisms in the regulation of slow electrical activity of the smooth muscle cells of the ureter]. 244 40

1. The intracellular Na+ activity (aNai) of the smooth muscle cells from guinea-pig ureter has been measured using double-barrelled Na+-sensitive micro-electrodes. aiNa in modified Krebs solution at 35 degrees C was of a mean 7.4 +/- 2.9 mM (n = 32, S.D. of an observation), equivalent to a Na+ equilibrium potential (ENa) of +66.7 mV. Membrane potential (Em) was of a mean -50.8 +/- 4.6 mV. 2. Inhibition of the Na+ pump by application of ouabain or removal of external K+ (K+o) resulted in a restricted rise of aNai. The rate of rise was faster in the presence of ouabain (10(-4) M) but the stabilized aNai was not significantly different from that observed after the prolonged absence of K+o. The mean aiNa recorded after prolonged Na+ pump inhibition was 20.6 +/- 5.5 mM (n = 28), equivalent to an ENa of +39.6 mV. Neither removal of K+o after aNai had stabilized in the presence of ouabain nor application of ouabain after aNai had stabilized in K+-free solution caused a rise in aiNa, suggesting that the Na+ pump was fully inhibited by either procedure. 3. Reduction of Na+o resulted in a rapid fall in aiNa against the electrochemical gradient, both before and after Na+ pump inhibition. At each level of Na+o, aNai stabilized such that ENa remained approximately constant in either condition. Readdition of Na+o resulted in a rapid recovery of aNai. 4. Elevation of Ca2+o (at constant Na+o) caused a fall in aNai of much the same time course as that observed on reduction of Na+o, both before and after Na+ pump inhibition. The extent of the fall was dependent upon the initial aNai. Reduction of Ca2+o resulted in a rise in aNai. 5. Elevation of the external divalent cation concentration with Mn2+ or, to a lesser extent, Mg2+ reduced aiNa in the presence of a functional Na+ pump. But after prolonged exposure to ouabain or K+-free solution, elevation of Mg2+o had no effect on aiNa while application of Mn2+o caused a slow rise. These results suggest that Ca2+o affects aiNa in two ways. One is mimicked by Mg2+ and Mn2+ and is probably due to alteration of the Na+ leak. The other is a specific effect, revealed by Na+ pump inhibition. 6. It is concluded that aiNa can be maintained far from equilibrium in the absence of a functional Na+ pump. Several lines of evidence are discussed which indicate the participation of Na+-Ca2+ exchange in Na+ extrusion in this condition.
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PMID:Investigation of factors affecting the intracellular sodium activity in the smooth muscle of guinea-pig ureter. 244 70

1. After application of ouabain (10(-4) M), the intracellular Na+ activity (alpha iNa) of smooth muscle cells in the guinea-pig ureter stabilizes at a relatively low level which can be rapidly lowered by reduction of external Na+ (Na+o) or elevation of Ca2+o. Both these procedures also elicit a transient contracture. These observations have previously been interpreted as evidence for Na+-Ca2+ exchange. The presence of such an exchange mechanism has now been further investigated by measurements of alpha iNa, tension, ion analysis and 22Na efflux. 2. Ion analysis demonstrated that tissues were able to maintain a high cellular K+ content in the presence of ouabain, but slowly lost K+ and gained Na+ if K+o was also removed, as expected for an infinite outward gradient for K+ and a fully inhibited Na+ pump. 3. Tissues were only able to maintain a low cellular Na+ and high cellular K+ in the presence of ouabain if Ca2+ was present in the bathing solution. Reduction of Ca2+o to very low levels also caused a continual slow rise in alpha iNa in the presence of ouabain, provided that the prolonged depolarization caused by these low levels was prevented by elevation of Mg2+o. Alteration of the membrane potential by changing K+o at constant Na+o showed that alpha iNa decreased by about 1.2 mM for a 10 mV depolarization, within the range from -70 to -30 mV. 4. A small Ca2+o-activated 22Na efflux was observed in ouabain-treated tissues in the absence of Na+o. 40 mM-Ca2+ was not more effective at activating this efflux than was 2.5 mM-Ca2+, while 40 mM-Mg2+ was ineffective. Restoration of the normal Na+o caused a large increase in the rate of 22Na loss. 5. Application of Mn2+ in the presence of ouabain caused a slow rise in alpha iNa and a small decline in resting tension. The fall in alpha iNa on reduction of Na+o was slowed by the presence of Mn2+ (mean half-time increased from 1.7 to 5.0 min) and the concomitant contracture was almost abolished. These results are consistent with a Mn2+-induced inhibition of Na+-Ca2+ exchange. However, the fall in alpha iNa induced by elevation of Ca2+o was unaffected by the presence of Mn2+ and the attendant contracture was, if anything, enhanced. 6. Observation of changes in alpha iNa and tension at various Mn2+ and Ca2+ concentrations demonstrated a competitive interaction between the two divalent cations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:An investigation of sodium-calcium exchange in the smooth muscle of guinea-pig ureter. 245 Oct 7

Lipoxygenase blocker BW755C has been studied for its effect on calcium inward current in intracellularly perfused voltage clamped and contraction of guinea-pig ureter smooth muscle. BW755C increased the Ca inward current in somatic membrane and inhibited contraction of the smooth muscle evoked by high-potassium solution. It is suggested that the effects observed are related to the changes in the level of cyclic nucleotides in cytoplasm due to the action of the final products of lypoxygenase breakdown of fatty acids from the cell membrane.
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PMID:[Effect of the lipoxygenase blockader BW755C on calcium currents in the nerve cell membrane of the snail and on the contractile responses of the ureteral smooth-muscle fibers in the guinea pig]. 245 56

An attempt was made to obtain electrophysiological evidence for continuous influx of Ca ion through voltage-dependent Ca channel (VDCC) in smooth muscle during long depolarization, for example in high K solution. Noninactivated Ca current [ICa(ni)] remaining after the accomplishment of voltage-dependent inactivation by prolonged depolarization for approximately 1 min was detected by three means under whole cell voltage clamp in several types of smooth muscle cells. The measurement of ICa(ni) was performed by micropuff application of Cd2+ or Ca2+ in the presence or absence of 5 mM extracellular Ca, respectively, or jump of extracellular Ca concentration [( Ca]o). The current-voltage relationship of ICa(ni) evaluated by these means had a peak at approximately -10 mV. The peak amplitude ranged from 5 to 25 pA, depending on whether the cells were isolated from guinea pig urinary bladder, ureter, vas deferens, taenia caecum, or rabbit portal vein. The ICa(ni) may be large enough to explain sustained contraction in high K solution, at least in these smooth muscle tissues. A window current simulated from the steady-state activation and inactivation curves and the maximum conductance of Ca current (ICa) in these cells suggests a theoretical basis for the observed ICa(ni).
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PMID:Measurement and simulation of noninactivating Ca current in smooth muscle cells. 246 90

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

1. The passive and active electrical properties of freshly dispersed single cells of the guinea-pig ureter were investigated using standard patch-clamp techniques. 2. Action potentials, having a rapid rising phase and a prolonged plateau, were recorded on passing depolarizing currents through the patch pipette when 'near-normal' physiological gradients were established across the cell membrane (5.9 mM-K+, 1.5 mM-Ca2+ in the bath; 126 mM-K+ in the pipette). 3. Under voltage clamp, depolarization to potentials positive of -50 mV (from a holding potential of -70 or -80 mV) triggered a net inward current which reached a peak in 5-10 ms and then slowly inactivated. 4. The averaged membrane current to depolarization to potentials between -30 and 0 mV showed two distinct patterns after the peak of the inward current; the membrane current either moved slowly outward over 400 ms or there was one or more transient outward currents superimposed on the slowly decreasing inward current. Both outward currents were blocked when 5 mM-tetraethylammonium (TEA) was added to the bathing solution, resulting in an increased inward current at all potentials. 5. Replacing the extracellular Ca2+ with Co2+ (1.5-5 mM) blocked the inward current and the outward currents to reveal another transient outward current (voltage activated) which activated rapidly to reach a peak within 5 ms and which inactivated exponentially with a time constant of 10 ms. This voltage-activated outward current was inactivated if the membrane was held at -50 mV, but could be reactivated by short hyperpolarizing pre-pulses. The amplitude of this transient current in response to a fixed depolarization (to 0 mV) was half-maximum when the hyperpolarizing pre-pulse was to -66 mV. The voltage-activated outward current was reduced in amplitude when the extracellular potassium was raised to 46 mM or upon exposure to 1 mM-4-aminopyridine (4-AP), but was not affected by 5 mM-TEA. 6. Replacing K+ in the pipette and bathing solution with caesium (Cs) blocked all outward currents, revealing the time course and voltage dependence of the inward current, which could be carried by Ca2+ or Ba2+ with little effect on its rate of inactivation. 7. It was concluded that the inward current recorded in single ureter cells was due to the flow of current through voltage-activated Ca2+ channels. The TEA-sensitive outward currents, whether transient or slowly activating, are presumably K+ channels activated by Ca2+.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Identification of the major membrane currents in freshly dispersed single smooth muscle cells of guinea-pig ureter. 260 Aug 37

1. Sodium-calcium exchange was studied in single enzymatically isolated cells of the guinea-pig ureter using the Ca2(+)-sensitive fluorescent dye Indo-1 to monitor the intracellular Ca2+ concentration ([Ca2+]i). Patch pipettes containing Indo-1 were used to introduce the dye into cells, to set the intracellular Na+ concentration ([Na+]i) and control the membrane potential during experiments. 2. With [Na+]i set at 11-12 mM and a membrane potential of -60 or -70 mV, brief depolarization of ureter cells elicited typical voltage-gated inward currents associated with rapid increases in [Ca2+]i which showed a bell-shaped potential dependence. If Ca2+ currents were blocked with nifedipine, depolarization led to slower rises in [Ca2+]i. The rates and amplitudes of these increased monotonically with progressively larger depolarizations up to +120 mV. 3. The nifedipine-resistant rises in [Ca2+]i elicited by depolarization were potentiated when the extracellular sodium concentration ([Na+]o) was reduced. Basal levels of [Ca2+]i also increased as [Na+]o was reduced, although the dependence of this effect on [Na+]o was smaller than would be predicted if [Ca2+]i was set only by a Na(+)-Ca2+ exchange process. 4. The nifedipine-insensitive rises in [Ca2+]i elicited by depolarization were potentiated at higher basal levels of [Ca2+]i. 5. The ability of cells to reduce [Ca2+]i rapidly following Ca2+ loading during voltage-gated transients was markedly inhibited if the Na+ concentration gradient was reversed, but was little affected if the Na+ gradient was decreased by 25 or 50%. Recovery from a Ca2+ load caused by reversal of the Na+ gradient could be induced by removal of Cao2+ in the continuing absence of Nao+, indicating the importance of a Na(+)-independent [Ca2+]i-lowering system. 6. The results demonstrate that Na(+)-Ca2+ exchange can modulate [Ca2+]i when [Na+]i and the membrane potential are set at or near their physiological levels in these smooth muscle cells. [Ca2+]i does not, however, appear to be markedly sensitive to the Na+ concentration gradient under the conditions employed for these experiments, suggesting that a Na(+)-independent Ca2+ extrusion system is mainly responsible for regulating [Ca2+]i under normal conditions.
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PMID:Alterations in [Ca2+]i mediated by sodium-calcium exchange in smooth muscle cells isolated from the guinea-pig ureter. 260 45

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