Mirtazipine/Remeron | Delayed menstruation | Herbal pain killer in
place of aspirin | Stuffy, blocked nose
taking Mirtazipine 15 mg for depression.
cause delayed menstruation?
herbal pain killer can I use in place of aspirin?
I'm also experiencing stuffy, blocked nose.
also a side effect of the med?
more sedating to be on a lower dosage than on a higher dose?
does this med behave in the same way as the benzos as in binding to
the GABA receptors?
function can affect menstrual cycle and Mirtazipine affects liver
pain killer you can use in place of aspirin is a patented extract
of maritime pine bark called Pycnogenol
blocked nose and flu syndrome (5%) are general side effects of Mirtazipine
like imipramine, may have a curvilinear dose-response curve. There
is some suggestion that sedation is more pronounced on low rather
than high dose mirtazapine therapy (15 versus 30 mg/day or more).
suggestion is principally based on the fact that there was a higher
incidence of sedation in the American trials, which used lower doses,
than in the European trials, which used higher doses of mirtazapine.
effect of mirtazapine at low doses is consistent with its high affinity
for the histamine-1 receptor.
that mirtazapine binds more avidly to that site of action than to
sites capable of mediating relief from a depressive episode, sedation
occurs at doses of mirtazapine below those needed for antidepressant
efficacy (i.e., less than 15 mg/day).
higher doses of mirtazapine result in the blockade of the alpha-2
adrenergic receptor, which produces an alerting or arousal effect
just like yohimbine and just the opposite of the sedation produced
by the alpha-2 adrenergic agonist, clonidine.
mirtazapine most likely causes sedation at low doses (i.e., concentrations)
by preferentially blocking the histamine-1 receptor, while at higher
doses (i.e., concentrations), mirtazapine blocks the alpha-2 adrenergic
receptor, which theoretically could reduce its sedating effects to
to the H 1 receptor, mirtazapine has very low affinity for the mACh
has no significant affinity for the 5-HT1A and 5-HT1B receptors.
works by blocking presynaptic a2-adrenergic receptors, which affect
serotonin and norepinephrine neurotransmission.
bind to a site located adjacent to the GABA receptor.
release onto TM neurons is modulated presynaptically by adrenergic
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