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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