Characterization of the Subtype of Presynaptic (α2-Adrenoceptors Modulating Noradrenaline Release in Cat and Bovine Cerebral Arteries

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Abstract
The possible existence of a heterogeneous population of α2-adrenoceptors (α2A and α2B, demonstrated by binding studies) in adrenergic nerve endings of cat and bovine cerebral arteries modulating noradrenaline release was investigated. Electrical field stimulation elicited an increase of tritium secretion from these vessels preincubated with (±)-[3H]noradrenaline, which was reduced by the α2-agonists, clonidine (1 μM) and B-HT 920 (0·01 and 0·1 μm), in cat cerebral arteries but only by B-HT 920 in bovine cerebral arteries. This reduction was inhibited by the antagonist of the α2B-subtype, prazosin, and the antagonists of α2A- and α2B-subtypes yohimbine and particularly rauwolscine. The effect of B-HT 920 was partially inhibited by clonidine in bovine, but not in cat cerebral arteries. In both types of arteries, prazosin, yohimbine and the α1-agonist methoxamine (all at 1 μm) failed to modify the stimulated radioactivity liberation, whereas it was increased by 1 μm rauwolscine, and by yohimbine plus prazosin in cat cerebral arteries. The basal tritium release was enhanced by rauwolscine and prazosin in cat cerebral arteries but only by the latter in bovine cerebral arteries. These results suggest: (1) the existence of presynaptic α2-adrenoceptors, mainly of the α2B-subtype, in these vessels negatively modulating noradrenaline release, their activity being greater in cat than in bovine cerebral arteries, and (2) clonidine has no agonistic but a weak antagonistic action in the latter vessels.

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