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  • 1985-1989  (3)
  • Periarterial field stimulation  (1)
  • Presynaptic α1-α2-adrenoceptors  (1)
  • Reaction center  (1)
Material
Years
  • 1985-1989  (3)
Year
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 332 (1986), S. 384-390 
    ISSN: 1432-1912
    Keywords: α,β-Methylene ATP ; SHR ; WKY-tail arteries ; Periarterial field stimulation ; Noradrenaline release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of α,β-methylene-adenosine triphosphate, (α,β-methylene ATP, a P2-receptor desensitising agent) have been evaluated on vasoconstrictor responses elicited by exogenous agonists or electrical field stimulation in isolated perfused SHR or WKY tail arteries and on tritium release elicited by electrical field stimulation in SHR-tail arteries pre-labeled with 3H-noradrenaline. Exposure to α,β-methylene ATP (0.1 μmol/l) significantly inhibited vasoconstrictor responses to electrical field stimulation in SHR tail arteries. These inhibitory effects were not further increased at a higher concentration of α,β-methylene ATP (1 μmol/l). In WKY tail arteries, α,β-methylene ATP (1 μmol/l) failed to significantly inhibit vasoconstrictor responses to electrical stimulation. In SHR tail arteries prelabelled with 3H-noradrenaline, α,β-methyleneATP (1 μmol/l) did not inhibit the stimulation evoked release of tritium. However, at this concentration, α,β-methylene ATP significantly antagonized the vasoconstrictor responses of SHR tail arteries induced by exogenous ATP (1 μmol/l), β,γ-methylene ATP (30 μmol/l), a stable agonist at P2-receptors, or 60 mmol/l KCl. These effects of α,β-methylene ATP on contractile responses to KCl were not observed in WKY-tail arteries. In tail arteries obtained from reserpine pretreated SHR, despite a 85–95% decrease in endogenous noradrenaline tissue content, the vasoconstrictor responses induced by periarterial field stimulation were greatly diminished, but not abolished. These residual responses to periarterial field stimulation were not antagonized by prazosin (0.1 μmol/l), but were practically abolished by the addition of α,β-methylene ATP (1 μmol/l). In tail arteries from WKY rats pretreated with reserpine, exposure to prazosin (0.1 μmol/l) further reduced the residual responses elicited by electrical field stimulation. In these WKY-tail arteries, addition of α,β-methylene ATP (1 μmol/l) did not further inhibit the remaining vasoconstrictor response obtained in the presence of prazosin. While our results suggest a significantly greater cotransmitter role for ATP with noradrenaline in tail arteries of SHR compared with control normotensive WKY rats, additional effects of α,β-methylene ATP not involving P2 receptors cannot be entirely excluded.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1912
    Keywords: Presynaptic α1-α2-adrenoceptors ; Idazoxan ; SHR tail arteries
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of several α-adrenoceptor antagonists have been examined on tritium release elicited by electrical stimulation from isolated perfused SHR tail artery preparations prelabelled with 3H-noradrenaline (3H-NA). Phentolamine and yohimbine potently facilitated the stimulation evoked release of tritium at low frequencies of stimulation, but the α2-adrenoceptor antagonist idazoxan was only weakly active at 1 μmol/l, despite antagonising the clonidine-evoked inhibition of 3H-release at a lower concentration of 0.1 μmol/l. The α1-adrenoceptor antagonists prazosin and corynanthine also increased stimulation evoked tritium release in this preparation, suggesting the presence of prejunctional α1-adrenoceptors. Furthermore, the α1-adrenoceptor agonist methoxamine (3 μmol/l) caused a significant inhibition of tritium-evoked release, an effect which was blocked by prazosin (10 nmol/l). When α1-adrenoceptors were blocked in the presence of prazosin, idazoxan (0.1 μmol/l) produced a significant facilitatory effect on the electrically-evoked release of 3H-transmitter. On the other hand, when α2-adrenoceptors were blocked in the presence of yohimbine, exposure to idazoxan (0.1 μmol/l) reduced significantly the stimulation-evoked release of tritium elicited by electrical stimulation. The results indicate that in the SHR tail arteries, idazoxan has a partial agonist inhibitory activity on transmitter release, which can mask the facilitatory effects due to blockade of presynaptic α2-adrenoceptors. The inhibitory effects of idazoxan appear to involve presynaptic α2-adrenoceptors, which when stimulated, reduce 3H-NA release in SHR tail arteries.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Photosynthesis research 10 (1986), S. 347-354 
    ISSN: 1573-5079
    Keywords: Photosynthesis ; Purple bacteria ; Reaction center ; Magnetic field ; Quinone reduction ; Triplet state
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Magnetic fields influence two properties of the P-870 triplet state observed in Rps. sphaeroides reaction centers: the yield of formation and the kinetics of decay. These effects have been studied in reaction centers which were prepared in three different states: state QA −, state QA 2− and state (− QA) (QA depleted). The triplet yields decrease with increasing magnetic fields, with B1/2's of about 140, 41 and 57 Gauss, respectively. The half-time of 3P-870 decay is not influenced by the field in state QA −; it increases at increasing fields, in state QA 2− and state (− QA), with the same B1/2 as the triplet yield. These results are discussed in the framework of current theories of the radical-pair dynamics and of the mechanism of triplet decay.
    Type of Medium: Electronic Resource
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