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  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Physiology 42 (1980), S. 429-439 
    ISSN: 0066-4278
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Biology
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 40 (1984), S. 1372-1373 
    ISSN: 1420-9071
    Keywords: Arteries, canine ; electrical stimulation ; contractile response ; aftereffects, persisting ; vibration, prolonged ; norepinephrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary 1–3 h after prolonged (3–16 h) vibration (120 Hz, 0.2–0.3 mm amplitude) of rings of canine saphenous arteries there was no significant change in the contractile response to electrical stimulation, exogenous norepinephrine or of neuronal uptake of tritium labeled norepinephrine. These results did not provide evidence for persistent aftereffects of prolonged vibration.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-7241
    Keywords: ouabain ; coronary artery ; norepinophrine ; beta-adrenoreceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ouabain, when applied to rings of the left ciroumfiex coronary artery of the dog (which contains both alpha1-adrenoceptors leading to contraction and beta1-adrenoceptors leading to relaxation) caused an initial contraction which peaked within 15 minutes and a later secondary increase in tension which peaked within 60 minutes. These contractions were prevented by Ca2+ removal or by verapamil. Adrenergic denervation with 6-hydroxydopamine did not affect the initial contraction. Thus it is due to a nonadrenergic effect of the glycoside. Since the secondary increase in tension was prevented by adrenergic denervation and prazosin, it is likely to be due to norepinephrine released from adrenergic nerves acting on alpha-adrenoceptors. This interpretation was confirmed by the finding that ouabain, after a latent period of about 35 minutes, augmented the output of 3H-norepinephrine from helical strips of the artery previously incubated with tritiated transmitter. In rings contracted with prostaglandin F2α, ouabain reduced beta-adrenergic relaxations caused by isoproterenol or exogenous norepinephrine, but not those caused by sodium nitroprusside. Thus, in this artery, ouabain depresses the response of the beta-adrenoceptors to the norepinephrine which it releases, thereby permitting the neurotransmitter to cause contraction by activating postjunctional alpha1-adrenoceptors.
    Type of Medium: Electronic Resource
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