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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In the epididymal portion of rat vas deferens, facilitation of noradrenaline release mediated by adenosine A2A receptors, but not that mediated by β2-adrenoceptors or by direct activation of adenylyl cyclase, was attenuated by blockade of α2-adrenoceptors and abolished by simultaneous blockade of α2-adrenoceptors, adenosine A1 and P2Y receptors. The adenosine A2A receptor-mediated facilitation was not changed by inhibitors of protein kinase A, protein kinase G or calmodulin kinase II but was prevented by inhibition of protein kinase C with chelerythrine or bisindolylmaleimide XI. Activation of protein kinase C with phorbol 12-myristate 13-acetate caused a facilitation of noradrenaline release that was abolished by bisindolylmaleimide XI and reduced by antagonists of α2-adrenoceptors, adenosine A1 and P2Y receptors. Activation of adenosine A2A receptors attenuated the inhibition of noradrenaline release mediated by the presynaptic inhibitory receptors. This effect was mimicked by phorbol 12-myristate 13-acetate and prevented by bisindolylmaleimide XI. It is concluded that adenosine A2A receptors facilitate noradrenaline release by a mechanism that involves a protein kinase C-mediated attenuation of effects mediated by presynaptic inhibitory receptors, namely α2-adrenoceptors, adenosine A1 and P2Y receptors.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 32 (2005), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The aim of the present study was to compare ecto-nucleotidase activities in rat bisected vas deferens using 1,N6-etheno(ε)-nucleotides (ε-ATP and ε-AMP) as substrates. Degradation was estimated by measuring the disappearance of the substrate and the appearance of its metabolites using HPLC with fluorescence detection. Incubation of tissue preparations (prostatic or epididymal portions) with 300 nmol/L ε-ATP at 37°C caused a partial disappearance of ε-ATP and appearance of its metabolites (ε-ADP, ε-AMP and ε-adenosine). Incubation at 25°C reduced ε-ATP degradation more in the prostatic than in the epididymal portion.2. Incubation of tissue preparations with ε-AMP at 37°C resulted in the disappearance of ε-AMP and the appearance of ε-adenosine, which was more pronounced in the epididymal than in the prostatic portion. Incubation at 25°C reduced ε-AMP degradation more in the epididymal than in the prostatic portion.3. Decreasing pH from 7.4 to 6.5 enhanced ε-AMP degradation only in the prostatic portion, whereas increasing pH from 7.4 to 8.5 enhanced ε-AMP degradation in both portions, but more markedly in the epididymal portion. The alkaline phosphatase inhibitors levamisole (10 mmol/L) and β-glycerophosphate (10 mmol/L) reduced ε-AMP degradation only in the epididymal portion.4. In conclusion, the results of the present study are compatible with the presence, in the bisected rat vas deferens, of an ecto-nucleotidase system that is involved in the degradation of extracellular purines, which may differ between the epididymal and prostatic portions, with the epididymal portion presenting a different and higher capacity to form adenosine.
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  • 3
    ISSN: 1432-1912
    Keywords: Noradrenaline-ATP cotransmission ; Noradrenaline release ; ATP release ; Isoprenaline Salbutamol ; Terbutaline ; Prejunctional ; β2-adrenoceptors ; Guinea-pig vas deferens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Activation of prejunctional β-adrenoceptors has been suggested to increase the release of noradrenaline but to decrease the neural release of ATP in the guinea-pig vas deferens. Experiments were carried out to determine the subtype of β-adrenoceptor involved. In [3H]-noradrenaline-preincubated tissues superfused with medium containing prazosin and suramin, isoprenaline (1–100 nM), salbutamol (0.01–1 μM) and terbutaline (0.1–10 μM) increased the overflow of tritium but reduced the overflow of ATP elicited by electrical stimulation (210 pulses/7 Hz). The effects of isoprenaline were blocked by the β2-selective antagonist 1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI 118,551; 100 nM). In prazosin- and suramin-free medium, isoprenaline (100 nM) did not change the overflow of ATP elicited by exogenous noradrenaline (10 μM). Isoprenaline (1–100 nM), salbutamol (0.01–1 μM) and terbutaline (0.1–10 μM) reduced the initial twitch contraction elicited by electrical stimulation (210 pulses/7 Hz) in prazosin-and suramin-free medium as well as the isolated purinergic neurogenic contraction obtained by exposure to prazosin. They increased or tended to increase the secondary sustained contraction elicited by electrical stimulation in prazosin- and suramin-free medium as well as the isolated adrenergic neurogenic contraction obtained in the presence of suramin. The inhibition by isoprenaline of the isolated purinergic contraction was attenuated by ICI 118,551 (100 nM) but not by the β1-selective antagonist 1-[2-((3carbamoyl-4-hydroxy)phenoxy)ethylamino]-3-[4-(1-methyl4-trifluoromethyl-2-imidazolyl)phenoxy]-2-propanol (CGP 20712A; 100 nM). The results confirm the opposite β-adrenoceptor-mediated modulation of noradrenaline and neural ATP release in the guinea-pig vas deferens. They show that the prejunctional β-adrenoceptor is of the β2 subtype.
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  • 4
    ISSN: 1432-1912
    Keywords: Noradrenaline release ; ATP release ; Cotransmission ; Isoprenaline ; Prejunctional ; β-adrenoceptors ; Guinea-pig vas deferens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Effects of isoprenaline on contraction, release of noradrenaline and release of ATP elicited by electrical field stimulation (210 pulses, 7 Hz) as well as on contractions elicited by exogenous noradrenaline and ATP were studied in the isolated vas deferens of the guinea pig. Release of noradrenaline was assessed as overflow of total tritium after preincubation with [3H]-noradrenaline. ATP was measured by means of the luciferin-luciferase technique. In [3H]-noradrenaline-pretreated tissues, electrical stimulation elicited an overflow of tritium and ATP and a biphasic contraction. Isoprenaline (1–100 nM) reduced the contraction, mainly phase I, and enhanced the evoked overflow of tritium; evoked overflow of ATP was not changed significantly. No, or almost no, contraction remained in [3H]-noradrenaline-pre-treated tissues exposed to both prazosin (0.3 μM) and suramin (300 μM), and the evoked overflow of ATP was reduced by about 82%. Under these conditions, isoprenaline (1–100 nM) again enhanced the evoked overflow of tritium, but it now decreased the evoked overflow of ATP. Propranolol (1 μM), when added on top of prazosin and suramin, prevented the effects of isoprenaline (1–100 nM). In some tissues not pretreated with [3H]-noradrenaline, purinergic and adrenergic components of the neurogenic contraction (again to 210 pulses, 7 Hz) were isolated by exposure to prazosin (0.3 μM) and suramin (300 μM), respectively. Isoprenaline (1–100 nM) decreased the isolated purinergic component but did not change significantly the isolated adrenergic component. Contractions elicited by ATP (1000 μM) were not changed and contractions elicited by noradrenaline (100 μM) were slightly increased by isoprenaline (1–100 nM). Isoprenaline (100 nM) did not change the degradation of ATP (100 μM) by pieces of the vas deferens. It is concluded that, in the guinea-pig vas deferens, activation of prejunctional β-adrenoceptors modulates the neural release of noradrenaline and ATP in opposite directions: release of noradrenaline is enhanced, whereas release of ATP is decreased.
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  • 5
    ISSN: 1432-1912
    Keywords: Guinea-pig vas deferens ; Hypogastric nerve stimulation ; Field stimulation ; ATP release ; Noradrenaline release ; Cotransmission
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Contractions and overflow of tritium and ATP elicited by hypogastric nerve stimulation (HNS) and field stimulation (FS) were studied in the guinea-pig isolated vas deferens preincubated with [3H]-noradrenaline. ATP was measured by means of the luciferin-luciferase technique. HNS and FS elicited contraction, tritium overflow and ATP overflow. HNS at supramaximal current strength produced smaller responses than did FS at supramaximal current strength (210 pulses/7 Hz). Supramaximal HNS and submaximal FS were used in the remainder of the study. Prazosin (0.3 μmol/l) reduced contractions and the overflow of ATP elicited by both HNS and FS; the evoked overflow of tritium was not changed (210 pulses/7 Hz). Combined administration of prazosin (0.3 μmol/l) and suramin (300 μmol/l) abolished contractions and reduced the overflow of ATP elicited by both HNS and FS slightly more than did prazosin alone; tritium overflow again was not changed (210 pulses/7 Hz). Contractions, tritium overflow and ATP overflow increased with the frequency of both HNS and FS (from 7 to 25 Hz; 210 pulses); the increase in ATP overflow with frequency was more marked than the increase in tritium overflow. The preferential increase of ATP overflow with the frequency of HNS and FS persisted in the combined presence of prazosin (0.3 μmol/l) and suramin (300 μmol/l). The study confirms for HNS, a more physiologic way of sympathetic nerve stimulation, several observations previously obtained with FS. First, HNS-evoked ATP release is detectable as an overflow of ATP into the superfusion fluid. Second, a large part of the HNS-evoked release of ATP is postjunctional in origin, due to activation of post-junctional α1-adrenoceptors and presumably P2-purinoceptors. Third, the average neural release of ATP per pulse facilitates with the frequency of stimulation to a greater extent than the average release of noradrenaline per pulse.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 555-560 
    ISSN: 1432-1912
    Keywords: Key words Rat vas deferens ; Evans blue ; ATP ; α ; β-Methylene ATP ; P2X-Purinoceptor ; Ecto-nucleotidase ; ATP overflow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The effect of Evans blue on nucleotide breakdown, nucleotide-evoked contractions and electrically evoked contractions, overflow of ATP and overflow of tritium (after labelling with [3H]-noradrenaline) was studied in rat vas deferens. Pieces of vas deferens degraded 83 to 85% of added ATP, ADP and 2-methylthio ATP (all 100 μM) over 30 min. Evans blue (100 μM) reduced this degradation to 22 to 26%. Nucleotides elicited contraction with potency declining in the order α, β-methylene ATP〉2-methylthio ATP〉ATP〉ADP. Evans blue (100 μM) shifted the concentration-response curve of α, β-methylene ATP to the right and increased the maximum. Concentration-response curves of ATP, ADP and 2-methylthio ATP, in contrast, were shifted to the left and responses were much potentiated. In the presence of Evans blue, the rank order of potency was ATP〉2-methylthio ATP〉α, β-methylene ATP 〉ADP. Electrical field stimulation (100 pulses at 10 Hz) elicited contraction and an overflow of tritium and ATP. Evans blue (100 μM) did not alter the contraction and the evoked overflow of tritium but increased 24-fold the evoked overflow of ATP. The results indicate that Evans blue may serve as an - albeit impure - ecto-nucleotidase inhibitor in functional experiments. Such experiments demonstrate that the low potency of ATP (and also ADP and 2-methylthio ATP) in eliciting contraction, and the small size of the overflow of ATP upon sympathetic nerve stimulation, are due to rapid breakdown.
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 555-560 
    ISSN: 1432-1912
    Keywords: Rat vas deferens ; Evans blue ; ATP α,\-Methylene ATP ; P2X-Purinoceptor ; Ecto-nucleotidase ; ATP overflow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of Evans blue on nucleotide breakdown, nucleotide-evoked contractions and electrically evoked contractions, overflow of ATP and overflow of tritium (after labelling with [3H]-noradrenaline) was studied in rat vas deferens. Pieces of vas deferens degraded 83 to 85% of added ATP, ADP and 2-methylthio ATP (all 100 μM) over 30 min. Evans blue (100 μM) reduced this degradation to 22 to 26%. Nucleotides elicited contraction with potency declining in the order α, \-methylene ATP 〉 2-methylthio ATP 〉 ATP 〉 ADP. Evans blue (100 μM) shifted the concentration-response curve of α, \-methylene ATP to the right and increased the maximum. Concentration-response curves of ATP, ADP and 2-methylthio ATP, in contrast, were shifted to the left and responses were much potentiated. In the presence of Evans blue, the rank order of potency was ATP 〉 2-methylthio ATP 〉 α, \-methylene ATP 〉 ADP. Electrical field stimulation (100 pulses at 10 Hz) elicited contraction and an overflow of tritium and ATP. Evans blue (100 μM) did not alter the contraction and the evoked overflow of tritium but increased 24-fold the evoked overflow of ATP. The results indicate that Evans blue may serve as an — albeit impure — ecto-nucleotidase inhibitor in functional experiments. Such experiments demonstrate that the low potency of ATP (and also ADP and 2-methylthio ATP) in eliciting contraction, and the small size of the overflow of ATP upon sympathetic nerve stimulation, are due to rapid breakdown.
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 367-371 
    ISSN: 1432-1912
    Keywords: Noradrenaline release ; Prejunctional adenosine receptors ; Endogenous adenosine ; Rat vas deferens ; A1-adenosine receptor ; A2-adenosine receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study aimed at determining the modulation by adenosine of the release of noradrenaline in the epididymal portion of the rat vas deferens. The tissues were treated with pargyline and perifused in the presence of desipramine and yohimbine. Up to four periods of electrical stimulation were applied (5 Hz, 9 min). The A1-adenosine receptor selective agonist R-N6-phenylisopropyladenosine (R-PIA; 100–900 nmol·l−1) reduced, whereas the A2A-receptor selective agonist 2-p-(2-carboxyethyl)phenethylamino-5′-N-ethylcarboxamidoadenosine (CGS21680; 3–30nmol·l−1) increased the electrically-evoked noradrenaline overflow in a concentration-dependent manner. The nonselective agonist 5′-N-ethy1carboxamidoadenosine (NECA; 30–300 nmol·l−1) reduced noradrenaline overflow, but the effect did not depend on the concentration. Adenosine deaminase at the concentration of 0.5 μ·ml−1 decreased but at that of 2.0 μ·ml−1 increased noradrenaline overflow. The inhibitors of adenosine uptake, S-(4-nitrobenzyl)-6-thioinosine (NBTI; 50 nmol·l−1) and dipyridamole (3 μmol·l−1), increased the electrically-evoked noradrenaline overflow. The A1-adenosine receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 20 nmol·l−1) caused an increase whereas the A2-adenosine receptor antagonist 3,7-dimethyl-1-(2-propynyl)xanthine (DMPX; 0.1 μmol·l−1) caused a decrease. NBTI (50 nmol·l−1), partially antagonized the effect of both DPCPX (20 nmol·l−1) and DMPX (0.1 μmol·l−1). It is concluded that, in the epididymal portion of the rat vas deferens, endogenous adenosine tonically modulates the release of noradrenaline evoked by electrical stimulation, through activation of both inhibitory (A1) and facilitatory (A2A) adenosine receptors.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 60-66 
    ISSN: 1432-1912
    Keywords: Release of taurine ; Noradrenaline ; Rat vas deferens ; ATP ; P2X-purinoceptors ; Cotransmission α,\-Methylene ATP ; Suramin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Release of taurine evoked by electrical stimulation (2700 pulses; 5 Hz; 10 mA unless stated otherwise) and its dependence on noradrenaline and ATP was studied in isolated, perifused rat vas deferens. Outflow of noradrenaline was also measured in some experiments. The basal outflow of taurine averaged 3.90±0.32 nmol/g tissue per min. Electrical stimulation increased the outflow to about 4 times basal values. The electrically-evoked overflow averaged 128.0±11.7 nmol/ g. An increase in current strength to 40 mA increased the evoked overflow by about 50%. At either current strength, the evoked overflow of taurine (and noradrenaline) was abolished by tetrodotoxin. Ca2+-deprivation blocked the overflow of taurine elicited by 10 mA and increased the overflow elicited by 40 mA pulses (but abolished noradrenaline overflow under either condition). Neither prazosin nor pretreatment of the rats with reserpine reduced electrically-evoked overflow of taurine (although reserpine pretreatment abolished evoked noradrenaline overflow). Tyramine (100 μmol/1; 9 min) caused an overflow of taurine 36% of that caused by electrical stimulation (but an overflow of noradrenaline 3 times higher than that evoked by electrical stimulation). Exogenous noradrenaline (9 min) caused a concentration-dependent overflow of taurine with a maximal effect at 162 μmol/1, amounting to 33% of the electrically-evoked overflow. α,\-Methylene ATP (19 μmol/1) elicited an overflow of taurine that faded despite continued exposure to the drug and amounted to 62% of the response to electrical stimulation. Thirty minutes after the start of application of α, \.-methylene ATP, electrically-evoked overflow of taurine was greatly reduced. Suramin (100 μmol/1) also reduced taurine overflow in response to electrical stimulation. It is concluded that electrical (neural) stimulation releases taurine in rat vas deferens. The release is mainly postjunctional in origin, secondary to ATP release from sympathetic axon terminals, and a consequence of postjunctional P2x-purinoceptor activation.
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  • 10
    facet.materialart.
    Unknown
    In:  http://aquaticcommons.org/id/eprint/8842 | 403 | 2012-06-12 17:53:25 | 8842 | United States National Marine Fisheries Service
    Publication Date: 2021-06-28
    Description: Ghost fishing is the term used to describe the continued capture of fish and other living organisms after afisherman has lost all control over the gear. Traps may be lost for a variety of reasons including theft, vandalism,abandonment, interactions with other gear, fouling on the bottom (i.e., traps and ropes are caught on rocky substrate), bad weather, and human error (Laist, 1995). Annual trap loss can be as high as 20% to 50% of fished traps in some fisheries (Al-Masroori et al., 2004). Because lost traps can continue to fish for long periods, albeitwith decreasing efficiency over time (e.g., Smolowitz, 1978; Breen, 1987, 1990; Guillory, 1993), ghost fishing isa concern in fisheries worldwide.
    Keywords: Biology ; Ecology ; Fisheries
    Repository Name: AquaDocs
    Type: article , TRUE
    Format: application/pdf
    Format: application/pdf
    Format: 321-327
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