The Contribution of cocoa additive to cigarette smoking addiction

Page 164 of 207 RIVM report 650270002
Octopamine
false adrenergic neurotransmitter agent and thus account for part or all of the
hypotensive action of monoamine oxidase inhibitors like pargyline (18).
heart rate: no data available.
Renal system
diuresis: Octopamine was administered in doses ranging between 25-200 µg/min
(1.6-20 µg/kg/min) both i.v. and into one renal artery of anaesthetized dogs.
Octopamine was hypertensive in doses of 100 µg/min and more and this change
was associated with a significant decrement in glomerular filtration rate (GFR)
and renal perfusion. This amine also exerted a direct tubular effect since it
decreased excretion of sodium and water and occurred in the absence of blood
pressure or renal perfusional changes when given i.v.. When given into one renal
artery octopamine produced only an ipsilateral antidiuresis and antinatriuresis, in
the absence of any change to GFR or renal perfusion. Lithium clearances suggest
that octopamine acts beyond the proximal tubule in altering the tubular
reabsorption of salt and water. Because octopamine was found to increase blood
pressure in the presence of a hypertensive infusion of noradrenaline, it is likely
that this amine exerts a primary pharmacological effect rather than liberating
noradrenaline from nerve terminals (19). An infusion of octopamine (220
µg/kg/min) in rats was associated with an increase in mean arterial pressure,
urinary volume, urinary Na and K output and their filtration fractions. Contrary
to the experiments on dogs, the glomerular filtration rate and renal plasma flow
were not affected in rats. A sudden and marked decrease in mean blood pressure
and diuresis was observed after stopping octopamine infusion (20).
saluresis: see diuresis.
Nervous system
central nervous system: Administration of octopamine by
intracerebroventricular (i.c.v.) or intrathecal (i.t.) routes, but not orally, produced
antinociception in the acetylcholine-induced abdominal constriction test (ED50 =
24.8 and 3.6 µg, respectively). Likewise, i.c.v. and i.t., but not peripheral (up to
200 mg/kg s.c.), administration increased latency in the 48 ºC hot-plate test
(ED50 = 11.5 µg i.c.v. and 0.2 µg i.t.). These actions were relatively long-lasting
and not blocked by naloxone. Antinociception following i.c.v. administration was
abolished in reserpinized mice or by pretreatment with i.t. phentolamine (2 µg).
These results suggest a moderate antinociceptive action of octopamine involving
non-opioid, reserpine-sensitive, central pathways (21).
Octopamine (50-250 µg) given intracerebroventricularly (icv) antagonized the
head twitch response induced in the rat by 5-hydroxytryptophan or 5methoxytryptamine,
and hyperthermia induced by quipazine (serotonin agonist) in
rats kept at high ambient temperature. Octopamine significantly depressed the
cerebral level of serotonin, and reduced the concentration of 5hydroxyindoleacetic
acid. Octopamine depressed the serotonin turnover rate.
These results indicate that octopamine given icv to rats antagonizes the central
serotonergic system (22).
In a study, the behavioral and neurochemical effects of intraventricular infusions
of octopamine (3,200 µg), tryptophan (800 µg), and octopamine plus tryptophan
delivered over 6 hours was studied in rats after performing a portacaval