Effect of the adrenergic neurone blocker, beta-TM10, on the depletion of noradrenaline induced by denervation or reserpine.

Abstract

The noradrenaline content of the rat submaxillary gland was determined fluorimetrically as various times after sympathetic denervation as well as after the subcutaneous injection of reserpine (300 μg/kg). The effect of an adrenergic neurone blocker (β-TMIO) was compared with that of an inhibitor of monoamine oxidase (pargyline). 2 Both βTM10 (50 mg/kg s.c. given 6 hours and repeated 12 hours after the operation) and pargyline (100 mg/kg i.p. at the operation) delayed the decline of endogenous noradrenaline observed after denervation; the delay was similar for both treatments. 3. Both,β-TM10 (50 mg/kg s.c. 2 hours before reserpine) and pargyline (100 mg/kg s.c. 6 hours before reserpine), caused a similar delay in the reserpine-induced decline of endogenous noradrenaline in the sympathetically decentralized gland. 4. Reserpine induced a higher rate of depletion in normal than in decentralized glands of untreated or pargyline-pretreated rats. However, the relation of depletion rates was reversed afterβ-TM10. 5. It is concluded that the last mentioned effect is at least partly due to the adrenergic neurone blocking effect ofβ-TMIO. The antagonism byβ-TMIO of the depleting effect of sympathetic denervation and of reserpine, on the other hand, is attributed to the ability of adrenergic neurone blocking agents to block monoamine oxidase. The results confirm earlier studies and indicate that the ability of adrenergic neurone blocking agents to block intraneuronal monoamine oxidase accounts for effects which up to now have been ascribed to their ability to prevent the release of noradrenaline by nerve impulses.