I was just doing some background research on tizanidine before trying (for medical condition).. & felt it necessary to just correct an obvious error here:
I find it weird that an adrenic agonist provides sleep.
First, just b/c it's an
ADRENERGIC drug, this does NOT mean whatsoever that it is an agonist or antagonist one way or another at adrenergic receptors. It just means it interacts w/ the adrenergic complex (for comparison: a lot of antipsychotics, as well as the antidepressant mirtazapine (Remeron, brand name) act as
antagonists at dopamine receptor subtypes.. BUT, they're "dopaminergics"..
just like cocaine, which is a dopamine-releasing-agent w/ quite opposite effects). What you are
really overlooking is the fact that
selectivity for certain subtypes/subunits--or certain "kinds"--of receptors cause differing effects (I gave you one example above w/ cocaine, here's another: agonists at the kappa subtype opioid receptor (i.e., Salvia) causes quite opposing, odd, and very-much-DIFFERENT effects than agonists at mu-subtypes of the opioid receptor (i.e., morphine).. Should it be "weird" that these effects are different? or that morphine doesn't make you hallucinate).
And yes, tizanidine most certainly acts as an agonist at a particular
kind of adrenergic receptors. But, you're missing the fact that it is highly
selective for the alpha-2 subtype of adrenaline receptors (as are clonidine, detomidine, dexmedetomidine: all of which are anti-hypertensives, cause sedation, & even analgesia. Another, Guanfacine, is particularly utilized here in the US to treat anxiety, PTSD, & hypertension). Conversely, look at antagonists at this receptor: including, but not limited to, stimulants like YOHIMBE. So generally, agonists of this particular subtype create sedation, hypotension, & muscle relaxation. Your question just seems way off the mark here: I mean, should we all assume SSRIs & MDMA create similar effects b/c they're both serotonergic agonists (or akin to the effects of an agonist, i.e., reuptake inhibition mechanism)? No. SSRIs have more selectivity at certain serotonergic subunits/subtype receptors--which cause some SSRIs (depending on its affinity to which subunit or type) to even cause drowsiness & act as a minor anxiolytic. Being an agonist is not akin how natural norepinephrine or epinephrine would plug into all these receptors. Nor does it mean that general adrenergics all have similar effects (methamphetamine is an adrenergic). Think of psychedelics: their effects are mainly from
highly selective agonist action at the subtype serotonin receptor of 5-HT2a (a few others too); but do other highly selective serotonergics cause such effects? No. SSRIs sure don't. Other serotonergic acting antidepressants sure don't.
...However, i'm not entirely convinced myself the full scope of tizanidine's pharmacological profile is known. (apologies to any of you biochems out there for using "subunit" and "subtype" interchangeably, i didn't feel that their minor differences were relevant for this post)