Presynaptic α2‐adrenoceptor antagonism by verapamil but not by diltiazem in rabbit hypothalamic slices
Open Access
- 1 March 1983
- journal article
- research article
- Published by Wiley in British Journal of Pharmacology
- Vol. 78 (3), 571-577
- https://doi.org/10.1111/j.1476-5381.1983.tb08817.x
Abstract
1 Rabbit hypothalamic slices prelabelled with [3H]-noradrenaline and superfused with Krebs solution were stimulated electrically at a frequency of 5 Hz. Exposure to verapamil (0.1 to 10 μm) significantly increased, in a concentration-dependent manner, the electrically-evoked overflow of tritium, without affecting the spontaneous outflow of radioactivity. 2 Exposure to diltiazem in concentrations up to 100 μm had no effect on the electrically evoked release of [3H]-noradrenaline, but increased the basal outflow of radioactivity at 10 and 100 μm. 3 The preferential α2-adrenoceptor antagonist, yohimbine (0.1 μm) significantly antagonized the inhibitory effect of clonidine or adrenaline on [3H]-noradrenaline overflow elicited by electrical stimulation. Verapamil (3 μm) also antagonized this inhibitory effect of the α2-adrenoceptor agonists on [3H]-noradrenaline release. In contrast to these results, exposure to diltiazem (10 μm) was ineffective in blocking the action of the α2-adrenoceptor agonist. 4 These results suggest that the two Ca2+-antagonists verapamil and diltiazem differ in their ability to affect central noradrenergic neurotransmission. While verapamil is a relatively potent α2-adrenoceptor antagonist, diltiazem is devoid of presynaptic α2-adrenoceptor antagonist properties.This publication has 19 references indexed in Scilit:
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