The Contribution of cocoa additive to cigarette smoking addiction

Page 112 of 207 RIVM report 650270002
Tryptamine
rate, whilst the pure depressor response was accompanied by a decrease in heart rate.
Tryptamine, injected centrally, causes both increases and decreases in arterial blood
pressure and heart rate. The pressor response to tryptamine results from the activation
of central noncholinergic, methysergide-sensitive, receptor sites and the depressor
response to tryptamine may be due to a centrally induced reduction in sympathetic
nervous activity. It is tentatively suggested that tryptamine participates in the
physiological regulation of the cardiovascular system of the rat, as both a central
excitatory and inhibitory regulator (20). Tryptamine produces pharmacological
effects in man that are similar to those produced by LSD and other tryptamine
derivatives. The cardiovascular effect is tachycardia (19).
Renal system
diuresis: no data available
saluresis: no data available
Nervous system
central nervous system:
It is proposed that tryptamine induces behavioural effect as a result of antagonism of
central serotonin systems. It has been shown that serotonin antagonists blocked the
certain tryptamine mediated effects, suggesting the possibility of serotonin receptormediated
tryptamine responses (12). Tryptamine produces pharmacological effects in
man which are similar to those produced by LSD and other tryptamine derivatives.
The CNS effects are behavioral changes and hallucinations (19).
The effects of intraperitoneal administration of tryptamine to rats pretreated with
iproniazid, on the acquisition of an unsignalled one-way active avoidance task, were
examined. Tryptamine at 2.5 and 5 mg/kg significantly increased the number of trials
required to perform this task. The iproniazid pretreatment had no affect on
acquisition, or any other performance variable, of the task. The acquisition deficit
induced by tryptamine may involve a direct stimulation of central serotonin receptors
since it was not induced by systemically administered serotonin. This effect was
reversed by the serotonin antagonists methysergide and metergoline, but was not
affected by depletion of brain serotonin, with p-chlorophenylalanine, or by the
dopamine antagonist haloperidol (21). Tryptamine given via intracerebroventricular
(i.c.v.) injection to mice produced a significant hypothermia at a dosage above 1 µg.
The hypothermic effect of tryptamine was inhibited by methysergide whereas
ketanserin and p-chlorophenylalanine did not affect it. That study demonstrated that
the hypothermia induced by tryptamine i.c.v. was produced by direct activation of the
5-HT1 receptor (22). Tryptamine induces serotonin syndrome (head weaving and
hindlimb abduction) and head twitch in mice through induction of the serotonin (5-
HT1 and 5-HT2) receptors in the brain (23). When tryptamine was injected (2 – 16
µg/dose) into the paraventricular nucleus of the hypothalamus after pre-treatment
with a monoamineoxidase inhibitor or with serotonin, it induced an anorectic effect.
This effect may be due to a prolongation of the activity of serotonin resulting from
tryptamine competing with serotonin for the same reuptake system (24).
autonomic system:
No data available
Other
Tryptamine has been shown to increase a dose-related plasma glucagon level of mice,