Release of Norepinephrine from the Isolated Heart.

Turnover rate of brain 5‐hydroxytryptamine increased by D‐amphetamine

“…A possible explanaition for the increase in 5-HIAA is that these cholinergic drugs raise the level of free acetylcholine which in turn depolarizes serotonergic nerve terminals by an action analogous to the release of catecholamines in adrenal medulla (Douglas & Poisner, 1962) and of noradrenaline from sympathetic neurones in heart (Richardson & Woods, 1959;Haeusler, Thoenen, Haefely & Hurlimann, 1968) and spleen (Kopin, 1966). The data in Table 6 are in accord with this speculation, since the drugs which raised 5-HIAA might be expected also to increase the concentration of acetylcholine in brain.…”

A Muscarinic Mechanism Inhibiting the Release of Noradrenaline From Peripheral Adrenergic Nerve Fibres by Nicotinic Agents

“…By means of chemical and biological assay procedures, it was later shown that noradrenaline is the stimulant amine released from rabbit isolated hearts by acetylcholine (Richardson & Woods, 1959) and the nicotinic drug, dimethylphenylpiperazine (DMPP) (Lindmar & Muscholl, 1961); in the experiments on noradrenaline release after acetylcholine, atropine 10-6 g/ml.) was applied.…”

Action of cocaine and chronic sympathetic denervation on vagal escape

“…It has also been pointed out that 2I Phy. 200 H. A. CAMPOS AND P. R. URQUILLA acetylcholine liberates an adrenaline-like substance from cardiac tissues (Hoffman et al 1945), which has been identified as noradrenaline (Richardson & Woods, 1959;L6ffenholz, 1967). Since the stimulation of the peripheral end of the vagus in the atropinized dog induces cardioacceleration, the acetylcholine liberated at the nerve endings could be in turn liberating adrenergic amines from the heart (Hoffman et al 1945;Middleton, Middleton & Toha, 1949).…”