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  • 1
    Electronic Resource
    Electronic Resource
    Possible involvement of presynaptic α1-adrenoceptors in the effects of idazoxan and prazosin on 3H-noradrenaline release from tail arteries of SHR (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 354-361 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00500009
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Influence of neuronal uptake on the contribution of smooth muscle α2-adrenoceptors to vasoconstrictor responses to noradrenaline in SHR and WKY isolated tail arteries (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 332 (1986), S. 43-49 
    Details
    ISSN: 1432-1912
    Keywords: SHR and WKY tail arteries ; Postjunctional α-adrenoceptor subtypes ; Neuronal uptake blockade ; Idazoxan
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the selective α-adrenoceptor antagonists idazoxan (α2) and prazosin (α1) were examined on responses to exogenous noradrenaline and to sympathetic nerve stimulation in SHR and WKY rat isolated perfused proximal tail artery segments. The influence of inhibition of neuronal uptake with cocaine on the effects of these antagonists was also determined. The following results were obtained. 1. Prazosin (10 nmol/l) was equieffective in antagonising responses to exogenous noradrenaline and sympathetic nerve stimulation in both SHR and WKY arteries and the degree of antagonism was similar in either the presence or the absence of neuronal uptake inhibition. 2. In contrast to prazosin, the effects of idazoxan (100 nmol/l), on both exogenous noradrenaline and sympathetic nerve stimulation were dependent on the degree of inhibition of neuronal uptake. 3. In SHR arteries, the degree of antagonism of responses to exogenous noradrenaline by idazoxan (100 nmol/l) decreased progressively as the concentration of cocaine was increased to 4 and 40 μmol/l; in WKY arteries, even in the absence of cocaine, idazoxan (100 nmol/l) did not antagonise responses to exogenous noradrenaline. 4. In SHR arteries, the responses to sympathetic nerve stimulation were reduced to a lesser extent by idazoxan (100 nmol/l) when the concentration of cocaine was increased to 4 μmol/l than in the absence of cocaine. In WKY arteries, idazoxan (100 nmol/l) reduced the responses to sympathetic nerve stimulation in the absence of cocaine. However, this concentration of idazoxan increased the responses to nerve stimulation in the presence of cocaine. 5. Our results indicate that smooth muscle α2-adrenoceptors are present in SHR tail arteries, both intra-and extrajunctionally. It appears that these postjunctional α2-adrenoceptors are distributed unevenly across the vessel wall, with the density of α2-adrenoceptors being greater close to the lumen. By increasing the access of noradrenaline to the adventitial-medial border region where α1-adrenoceptors predominate, cocaine decreases the relative contribution of postjunctional α2-adrenoceptors to responses to both exogenous and endogenous noradrenaline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00633195
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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