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Physiological Contradiction Between Vasoconstriction and Pupil Dilation

Psychadelic_Paisly

Psychadelic_Paisly

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Hey, to all those in the know of physiology etc. I am curious as to why drugs that are vasocontrictor's (MDMA/Meth) cause pupil dilation... Isn't pupil dilation due to the DILATION of the blood vessels???
 
You have two sets of smooth muscle fibres that control the diameter of the pupil. The pupillary constrictor muscles are sphincters which cause the pupil diameter to decrease when they contract.

The second set, also smooth muscle are known as pupillary dilator muscles. These are connected radially to the outer edge of the pupil. When these muscles contract, the pupil is enlarged.

As for why these should be contracted by psychedelics and not be compensated by the constrictor muscles I have no idea
 
Pupilliary dilation is not caused by dilation of blood vessels, its caused by muscles dilating the pupil like PD said.

I'm not sure of the exact pharmacological reason, but the dilator muscles are part of the sympathetic (fight-or-flight) nervous system.

Adrenaline causes bronchial dilation in the lungs -- opening up the alveoli to allow better oxygen transfer into the blood. This is one of the reasons that adrenaline is given for anaphalactic shock.

It causes vasoconstriction to increase blood pressure. Higher blood pressure --> Blood oxygen transfers faster around the body, which is useful when you're trying to escape tigers.

Adrenaline also causes the pupils to dilate, to allow more light to enter the eye. This is useful if escaping predators at night -- you've got more of a chance of seeing them, and what's around you. There's a consequent tradeoff in loss of image clarity, but that's not particularly important when all you need to do is be able to detect things.
 
Of course, makes perfect sense VelocideX. It brings a whole new meaning to the term 'escapism' when referring to psychedelic or sympathomimetic drug use ;)
 
Yeah contraction of radial eye muscles causes pupil dilation. Comes from alpha1 adrenoceptor activation by noradrenaline release from consuming indirectly acting sympathomimetic drugs eg aphetamine/ephedrine/tyramine or direct ones like cocaine etc
 
*EDIT* The following comments are not mine, but a friend's who is about to begin an honours course in Biomedical Science...

the only thing that i know about alpha 1 adrenoceptors is that stimulation causes increased contraction of the cardiac muscle, resulting in increased heart rate. I understand that this is one of the affects of MDMA but i dont understand how stimulation of the alpha 1 adrenoceptors causes possible vasoconstriction. as far as i know there are no receptors of this type within the eye.
in the fight or flight response increasing blood supply to the peripheral circulation and to the eyes by VASODILATION results.
are you sure that vasoconstriction results from taking MDMA
 
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I always wonder about this.....espeically since I tend to dose up on smack (or codiene) after taking E.

Apart from the abuse i'm putting my poor heart through would the constricting of dilated pupils, enlarged by Adrenaline cause one problems, eye wise that is? Since i've got pretty bad eyesite in the first place its difficult for me to ascertain if any changeshave occurred
 
*EDIT* The following comments are not mine, but a friend's who is about to begin an honours course in Biomedical Science...

i dont think its the interaction of the two drugs on the pupils causing the problem. its more likely the CNS affects of the two drugs. i think that the affects of heroin result in problems interpreting information recieved from the peripheral sensors within the brain, but im not sure of the interacting affects of MDMA. you might be right in that the information received from the brain following pupil dilation (MDMA) is too much, causing a sort of brain overload
 
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peripheral vasoconstriction certainly is a documented effect.

Here's a study in rabbits:
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=11606652
J Neurosci. 2001 Nov 1;21(21):8648-54. Related Articles,Links

Cutaneous vasoconstriction contributes to hyperthermia induced by 3,4-methylenedioxymethamphetamine (ecstasy) in conscious rabbits.

Pedersen NP, Blessing WW.

Departments of Medicine and Physiology, Centre for Neuroscience, Flinders University, Bedford Park 5042, South Australia, Australia.

3,4-Methylenedioxymethamphetamine (MDMA; "Ecstasy") increases body temperature. This process could be associated with increased cutaneous blood flow, as normally occurs with exercise-induced hyperthermia. Alternatively, an MDMA-induced fall in cutaneous blood flow could contribute to the hyperthermia by diminishing normal heat transfer from the body to the environment. We investigated these possibilities by administering MDMA (1.5-6 mg/kg, i.v.) to conscious freely moving rabbits, determining effects on body temperature, cutaneous blood flow (measured by a Doppler ultrasonic probe that was chronically implanted around the ear pinna artery), and other cardiovascular parameters. MDMA caused a dose-dependent increase in body temperature (from 38.3 +/- 0.3 to 41.2 +/- 0.4 degrees C after 6 mg/kg; p < 0.01; n = 5), preceded and accompanied by a dose-dependent cutaneous vasoconstriction (from 29 +/- 6 to 5 +/- 1 cm/sec after 6 mg/kg; p < 0.01; n = 5). MDMA (3 mg/kg) did not change blood flow to the mesenteric vascular bed. Prior unilateral cervical sympathectomy reduced the increase in body temperature elicited by MDMA (6 mg/kg) from 2.0 +/- 0.2 to 1.3 +/- 0.2 degrees C (p < 0.01; n = 5). On the denervated side, ear pinna blood flow after MDMA injection was 13 +/- 3 cm/sec, compared with 3 +/- 1 cm/sec on the sympathetically intact side (p < 0.05; n = 5). Thus, sympathetically mediated cutaneous vasoconstriction is one mechanism whereby MDMA causes hyperthermia. Reversal of cutaneous vasoconstriction by appropriate pharmacological means could be of therapeutic benefit in humans suffering from life-threatening hyperthermia induced by MDMA.
Click to expand...
 
*EDIT* The following comments are not mine, but a friend's who is about to begin an honours course in Biomedical Science...

im really interested in reading the rest of the article. do you know if i can get access to a full copy of it?
 
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PP:... all your friend has gotta do is pick a BL nickname and give a working email address for the password ;)
 
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excuse me if i sound really dumb, but to put it in layman's terms - your pupils dilate because the muscles contract around it - is this because all the rest of your muscles contract on e, as an effect, so it is just like any other muscles so it contracts? does that make sense? and if that is the case, would taking magnesium make your pupils dilate less coz the muscles won't contract so much (just a random thought, if the above is true). i never knew that was why they dilated...very interesting.
 
As mentioned above by VelocideX, constriction of the radial muscles is due to adrenoreceptor stimulation. These receptors are located in ganglions.

Ganglions are nerve connection points. In this case, adrenalin (a neurotransmitter) is normally released in the brain in a manner termed sympathetic or parasympathetic response. The adrenalin or noradrenaline (NA) stimulates the ganglion.

Upon receiving the adreno 'signal', the ganglion activates another neurotransmitter system. This is the choline or acetylcholine system, which is also the system at work for any automatic response your body makes to stimulus.

An example is how a low light environment will increase pupil size by adrenorelease to the ganglion which controls the radial iris muscles.

But in a bright light situation the constrictor muscle is instead stimulated - again by an adreno - auto-response. Only this time the brain directs this by releasing NA to the ganglion which controls this muscle.

Some ganglions are a tad more complex in their operations but they bascially all work as relay points for the nervous system.
 
Now I could be wrong here, and this will probably teach me for being anal, but as far as I'm awear, Alpha1-adrenoreceptors, which are responsible for sympathomimetic (stimulants) and hallucinogen-induced pupillary dilation are located on the iris radial dilator muscle, and cause an increase in smooth muscle tone. The ganglion responsible for the neurons which release noradrenaline to stimulate adrenoreceptors are located in the paravertabrle sympathetic chain ganglia.

Meanwhile, parasympathetic ciliary ganglion (cranial nerve III) fires off acetylcholine onto the ciliary muscle, activating M3 receptors, causing increase tone, and constriction, contracting the pupil.

Could be wrong, but that's how I remember it.
 
Now I could be wrong here, and this will probably teach me for being anal, but as far as I'm awear, Alpha1-adrenoreceptors, which are responsible for sympathomimetic (stimulants) and hallucinogen-induced pupillary dilation are located on the iris radial dilator muscle, and cause an increase in smooth muscle tone
Click to expand...

No, you're correct BilZ0r, my mistake. It's my anatomy that's a little rusty. The radial muscle is contracted through alpha-adreno stimulation directly via receptors on the smooth muscle.
 
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