RELEASE OF 3H‐ADRENALINE FROM AN ISOLATED INTACT PREPARATION OF THE RABBIT ADRENAL GLAND: NO EVIDENCE FOR RELEASE MODULATORY α‐ADRENORECEPTORS

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Abstract
Catecholamine secretion from the rabbit adrenal gland may be subject to modulation by a mechanism involving .alpha.-adrenoreceptors in an isolated preparation of the gland. Intact left adrenal glands from the rabbit were perfused with Krebs-Henseleit solution through their vasculature. The adrenal catecholamine stores were radiolabeled with 3H-adrenaline [epinephrine] and subsequently, efflux of the radiolabel was elicited by stimulation of an attached segment of splanchnic nerve (60 s at 5 Hz). In some experiments, efflux of radiolabel was elicited by perfusion with K-enriched Krebs-Henseleit solution (30 mM). Radioactivity released in response to nerve stimulation was accounted for almost entirely by (3H)-adrenaline. Stimulation-induced (S-I) efflux was abolished by 0.1 .mu.M tetrodotoxin and by omission of Ca from the perfusion medium and was reduced by .apprx. 55% by 100 .mu.M hexamethonium. S-I efflux was enhanced to .apprx. 150% of control S-I efflux in the presence of 10 .mu.M phenoxybenzamine. Phentolamine 3 .mu.M and yohimbine in concentrations of 0.1 and 1.0 .mu.M had no effect. In a high concentration (10 .mu.M) yohimbine reduced S-I efflux by .apprx. 50%. The effect of phenoxybenzamine in enhancing S-I efflux may have been due to blockade of reuptake of 3H-adrenaline since cocaine (30 .mu.M) enhanced release to a similar extent. S-I efflux was not altered in the presence of the .alpha.-adrenoreceptor agonists noradrenaline [norepinephrine] (0.1 .mu.M), clonidine (1 .mu.M) or oxymetazoline (10 .mu.M). Release of radiolabel evoked by perfusion with 30 mM K solution was unaltered in the presence of phentolamine (3 .mu.M) or clonidine (1 .mu.M). These findings do not support the existence in the rabbit adrenal gland of a mechanism involving .alpha.-adrenoreceptors through which catecholamine secretion may be modulated.