Abstract
When rats and mice are treated with an inhibitor of noradrenaline (NA) synthesis (H 44/68, the methylester hydrochloride of dl‐α‐methyltyrosine) there is a reduction in the NA content in sympathetically innervated organs such as the heart and the submandibular glands. In the present investigation the mechanism behind this depletion has been examined by biochemical methods and with the histochemical fluorescence method of Falck and Hillarp. If the nerve impulse flow in the adrenergic nerves is reduced to a minimum by cutting the preganglionic trunk, the decrease in the transmitter content is reduced both in the iris and the submandibular gland. This shows that the nerve impulse flow in intact nerves is the main cause of the depletion of NA after treatment with an inhibitor of NA synthesis. When mice and rats are exposed to cold (3°C) after treatment with H 44/68 there is a significantly greater reduction in the NA content of the heart than when the animals are kept at room temperature (22°C) after the same treatment. This indicates that there is an increased nerve impulse flow in the adrenergic nerves of the heart in the animals exposed to cold stress. Uptake of adrenaline in the heart may also indicate an increase in activity in the adrenal medulla of these animals. There is good correlation between the biochemical and histochemical findings but the latter indicate that there is a greater reduction in the adrenergic nerves of the iris than in the nerves of the submandibular gland.The investigation shows that inhibitors of NA synthesis are very useful in functional studies of the adrenergic nerves.

This publication has 11 references indexed in Scilit: