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Flashcards in Autonomic Drugs Deck (44):


- direct acting adrenergic agonist
- non-selective
- IV, like all catecholamines

Epinephrine has many physiological effects in the body:
1. CV
Heart: beta1 receptors in heart - epinephrine increases HR and force of contraction --> increase SBP
Smooth muscles lining cells: alpha1 and beta2 receptors on smooth muscle cells - epinephrine increases vasoconstriction --> increases peripheral resistance --> increases DBP
--> Epinephrine will increase both systolic and diastolic pressure

Endogenous epinephrine can sometimes activate the beta2 receptor. At very low levels of epinephrine, epinephrine has higher binding affinity for beta2 than for alpha1. So at very low levels of epinephrine like you sometimes see with endogenous epinephrine you may only see activation of beta2 receptors and not activation of alpha1, which can cause vasodilation
But when using epinephrine as a drug, we always see occupation of both alpha1 and beta2 --> vasoconstriction.

2. Pulmonary
Epinephrine activates beta2 receptor --> bronchodilation on bronchial smooth muscle

3. Metabolic effects
Epinephrine activates beta2 receptors on hepatocytes and tells them to break down glycogen and release glucose into the blood

- stimulate the heart in cardiac emergencies
- serious hypersensitivity reactions, including anaphylaxis
- asthma
- co-administer with local anesthetics



- direct acting adrenergic agonist
- selective for both alpha and beta, specifically alpha1, alpha2, and beta1

Norepinephrine: only under certain circumstances is norepinephrine used in emergency situations. For some reason, large doses of exogenous norepinephrine can lead to slowing of the heart. It can be coadministered with local anesthetics though.



- direct acting adrenergic agonist
- selective for both alpha and beta, specifically alpha1 and beta1

Dopamine: increases SBP and DBP
Dopamine will also activate dopamine receptors located on renal arteries. In turn, renal arteries vasodilate --> maintains nice healthy blood flow to kidneys.
One potential problem of epinephrine in cardiac emergencies: vasoconstriction everywhere. And while epinephrine clearly gets the patient through the acute event, there is always a potential for other problems down the line because of vasoconstriction elsewhere. There are studies beginning to identify neurological deficits from compromised blood supply in brain. There is also concern for lack of blood flow to the kidneys. Dopamine = alternative to this.



- direct acting adrenergic agonist
- selective for both alpha and beta, specifically alpha1, beta1, beta2

Dobutamine - consists of 2 isomers that are given together to activate receptors in the heart. It is really just a beta1 agonist. It's a catecholamine that will only act at beta1 receptors on the heart and is only used in emergency situations in the hospital.
+ isomer: beta1 agonist, but also has alpha1 antagonist activity.
- isomer: alpha1 agonist.
Alpha1 antagonist activity of the + isomer cancels the alpha1 agonist activity of the - isomer.



- direct acting adrenergic agonist
- selective for alpha1 receptors only

Many uses:
- increase DBP via injection
- major use: nasal decongestant - aerosol you squeeze into nasal passages --> activate alpha1 receptors on the arterioles in the nasal mucosal and cause vasoconstriction --> increases volume/size of nasal mucosa so you get more air in and out of the nasal passages.
- get rid of blood shot eyes (eyedrops) --> vasoconstriction of blood vessels in the eye.
Gets rid of blood shot eyes but causes dilated pupils (alpha1 receptors located on the iris dilator muscle)



- direct acting adrenergic agonist
- selective for alpha2 receptors only

Clonidine - alpha2 agonist.
- used to treat chronic HTN
- given orally
- mechanism: in the CNS, clonidine activates alpha2 receptors --> decrease in sympathetic output from the brain --> decrease in SBP and DBP, heart rate, force of contraction, and vasodilation. Ignore what clonidine is doing in the periphery - attribute all of its effects to the CNS.
Clonidine is also used to treat people who are addicted to alcohol or opiates. This helps them get through withdrawal syndrome. A large component of withdrawal syndrome is an increase in sympathetic tone from the brain. Clonidine reduces sympathetic tone during withdrawal syndrome.

Clonidine lowers intraocular pressure in patients with high BP and glaucoma. Alpha 2 agonists decrease the rate of vitreous humor formation in the eye. So instead of being given systemically, clonidine can be given as eyedrops for these patients. However, it is irritating to the eye.

Therefore Brimonidine, another alpha2 agonist is used in eyedrops. It is not irritating to the eye.

--> alpha2 agonists are also used to treat glaucoma.



- direct acting adrenergic agonist
- selective for alpha2 receptors only
- eyedrop (non irritating to the eye) that decreases the rate of vitreous humor formation in the eye --> lowers intraocular pressure in patients with high BP and glaucoma



- direct acting adrenergic agonist
- selective for beta1 and beta2 receptors only

Isoproterenol - activates both beta1 and beta2 receptors. Can be used for asthma because it will activate beta2 receptors and cause bronchodilation. Similar problem that epinephrine has though - activates beta1 receptor of the heart, can feel the effects on the heart



- direct acting adrenergic agonist
- selective for beta2 receptors only

Albuterol - selective for beta2, don't see much activation of beta1 (will sometimes see though if concentration is high enough because they're selective, not specific)
generally inhaled via aerosol form



Ritodrine - discontinued, replaced by Terbutaline, also a beta2 agonist. It is used to suppress uterine contractions in premature labor.



- indirect acting adrenergic agonist
- releaser

- used therapeutically for ADHD, narcolepsy, and chronic fatigue syndrome. Can induce a feeling of euphoria at high levels - there is abuse potential. All CNS effects.

Amphetamine acts on Uptake 1 transporter and reverses the flow of norepinephrine. It is normally taken up back into the sympathetic neuronal varicosity, but amphetamine reverses this pump.
It does the same thing to the transporter in storage vesicle. It will pump the norepinephrine out of the storage vesicle, out of the varicosity to elevate norepinephrine levels at the neuroeffector junction.

--> should be able to predict what the peripheral effects of amphetamines are: activate beta1 receptors in the heart (increase in HR and contractility --> increased SBP)
Norepinephrine doesn't bind to beta2 receptor --> on smooth muscle they act 100% on alpha 1 --> vasoconstriction
--> increase peripheral resistance --> increase DBP
--> increase in SBP and DBP

At high doses of amphetamine, there is always a concern about ventricular arrythmias. Elevating norepinephrine levels in the neuroeffector junction at the heart always comes with some risk of inducing ventricular arrythmias (dangerous, very lethal)



- indirect acting adrenergic agonist
- releaser
- same mech as amphetamine, maybe safer
- for ADHD



- indirect acting adrenergic agonist
- releaser
- not a drug, natural breakdown product of tyrosine, consumed in different foods
- patients on MAOI cannot consume foods high in tyramine. if they do, there is a substantial increase in norepi.



- indirect acting adrenergic agonist
- uptake inhibitor
- blocks the uptake 1 transporter
- local anesthetic
It is the only local anesthetic that leads to its own vasoconstriction -
not given with norepinephrine or epinephrine because it upregulates norepinephrine at the site of injection


Tricyclic antidepressants

- indirect acting adrenergic agonist
- uptake inhibitor



- indirect acting adrenergic agonist
- inhibitor of metabolism



- mixed adrenergic agonist - acts like both direct and indirect acting

Ephedrine is used to treat incontinence (causes relaxation of detrusor muscle and constriction of internal urethral sphincter muscle.) It is sometimes used in the hospital to treat serious hypotension (can be injected or given orally)
The biggest issue we have with ephedrine comes from the fact that ephedrine is naturally occurring in certain plants and is contained in lots of nutritional supplements.
OTC use was banned by the FDA.
Cannot legally purchase any product with ephedrine in it in the US without prescription but the internet is a very powerful thing...
These are a problem. Patients with pre-existing CV disease take ephedrine containing supplements and end up with MI and strokes.



- adrenergic antagonist
- non-selective alpha adrenergic antagonist (alpha1 and alpha2)

If we block alpha 1 receptors like in phentolamine, we see vasodilation --> decrease in DBP

Alpha antagonists not only cause vasodilation in arteries/arterioles, they also cause vasodilation in venules --> shifts blood from arteriole side to venous side
--> decrease in venous return --> decrease in SBP
Phentolamine causes drop in SBP and DBP

It is used in emergency situations in hospitals to lower BP. It is not used chronically to treat HTN because 1. phentolamine will cause severe orthostatic hypotension since it blocks many alpha1 receptors and you need these on the arteries/arterioles to cause vasoconstriction in the baroreceptor reflex and 2. reflex tachycardia: phentolamine increases HR because it blocks alpha2 receptors in the heart --> more epinephrine comes out --> increase in HR

Same event occurs with vascular smooth muscle because there are alpha1 receptors there.
--> Elevated norepinephrine levels at vascular smooth muscle don't have any effect because phentolamine is blocking the alpha1 receptor.

But in the heart, you don't have alpha1 receptor on the effector cell, you have the beta1 receptor. Phentolamine doesn't block the beta1 receptor. When phentolamine blocks alpha2 in the heart, beta1 can be activated by increased norepinephrine --> increased HR
May also see an increase in the force of contraction, but not an increase in SBP because there is less blood for the heart to deal with - it's trying harder but there's less venous return. --> Phentolamine is only used in the hospital.



- adrenergic antagonist
- selective alpha1 adrenergic antagonist

Selective alpha blockers can be used chronically to treat HTN

Prazosin blocks alpha1 receptor -
doesn't increase the HR. Taken orally. Effectively lowers both SBP and DBP.
2 issues:
1. first dose effect - the first time you give Prazosin to the patient, it causes substantial orthostatic hypotension because it blocks many alpha1 receptors. However after the first dose, the orthostatic hypotension becomes much less of an issue. Degree decreases substantially or disappears altogether for some patients
--> deal with this by giving first dose of prazosin to patient at night.

2. epinephrine reversal - if a patient is taking an alpha1 blocker and now has a cardiac emergency which normally requires an injection of epinephrine, if these pts get epinephrine and alpha1 receptors are blocked, epinephrine that normally binds to alpha1 receptor binds instead to beta2 receptor --> causes more vasodilation, the exact opposite of what you want the epinephrine to do.
This however doesn't happen all the time because it depends on the dose of alpha1 blocker and the dose of epinephrine
In a cardiac emergency you want to use some other drug other than epinephrine - may want to use norepinephrine because it will not bind to beta2 receptor



- adrenergic antagonist
- selective alpha1a adrenergic antagonist

You find alpha1a receptors on the muscle capsule of the prostate. The prostate surrounds the urethra in males. in elderly men, you start to see hyperplasia of the prostate but can only expand so much because of the muscular capsule. When the muscular capsule begins to push back on the expansion of the prostate, the first thing that gets squeezed is the ureter --> difficulty in urination

Drugs like tamsulosin block the alpha1a receptor in the muscle on the prostate capsule --> muscle capsule relaxes and prostate can expand more to take pressure of the urethra



- direct adrenergic antagonist
- non-selective beta adrenergic antagonist (beta1 and beta2)
- first generation

Propranolol - used to treat chronic hypertension, given orally
Blocks the beta1 receptor --> HR goes down --> force of contraction goes down --> SBP goes down
Blocks the beta2 receptor (makes no sense) --> more vasoconstriction but that doesn't happen, you see vasodilation and decrease in DBP
Why? We don't know.

- angina - decrease the workload of the heart, slowdown HR, reduce force of contraction, reduce oxygen consumption by the heart muscle
- arryhythmias - at high doses
- MI - improve prognosis - if patient arrives in ER in the middle of the MI and give beta blocker, prognosis is good. Can take a beta blocker up to several hours after MI and can still cause a better prognosis.
- glaucoma - drop in intraocular pressure: by blocking beta2 receptors in the ciliary body in the eye, you can decrease the rate of formation of aqueous humor. Timolol (eye drop) is often used because it doesn't irritate the eye.
- migraines - beta blockers decrease freq and severity of migraines - don't know mechanism

potential issues:
1. asthmatics - never give them a non-selective beta blocker - never give drug that blocks beta2 receptor --> can precipitate asthma attack (need beta2 for relaxation of bronchial muscle for bronchodilation)
Blocking the beta2 receptor in non-asthmatic patient does nothing

2. also contraindicated in insulin-dependent diabetics - why?
We have 2 systems to keep glucose in our blood when we're hungry: 1. glucagon from the pancreas tells the liver to break down glycogen and release glucose into the blood and 2. epinephrine tells hepatocytes to breakdown glycogen and release glucose into the blood. You only need one of these.
In insulin-dependent diabetics, within the first 10 years of diagnosis, patients are usually not producing glucagon. This is not a big deal because you don't need glucagon as long as you have epinephrine to tell the liver to breakdown glycogen and release glucose. But what you can't do is block the beta2 receptor because that would prevent epinephrine from binding to beta2 receptor on hepatocytes. Since you have no glucagon to replace that, these patients cannot regulate their blood glucose levels. Anything that blocks beta2 receptor cannot be used for insulin-dependent diabetic.

3. Sudden withdrawal - you can get very serious consequences
when you have been taking a beta blocker chronically and you suddenly stop. When you have been blocking a receptor chronically, the beta receptors that you had been blocking will upregulate. Beta1 receptors in the heart will try and overcome the beta blockade - the cells have some ability to sense that something is being blocked and will try to overcome that but will not be able to overcome the effects of the drug. You could get doubling of beta1 receptors in the heart but as long as the patient takes the beta blocker there's no issue. Sudden withdrawal however will cause normal levels of epi and norepi but twice as many beta1 receptors that are not blocked anymore --> enormous increase in HR and force of contraction --> MI, hemorrhagic stroke
Patient needs to be slowly tapered off the drug so that the receptors can slowly come back to normal levels before the drug is completely terminated

4. Hyperthyroidism - beta blockers are sometimes used to suppress symptoms
In hyperthyroidism, the thyroid is producing much higher levels of T3 and T4. T3 and T4 help regulate the number of adrenergic receptors in various tissues. When you have an excess of T3 and T4, there is an increase in the number of adrenergic receptors located in many different tissues, including the heart. The beta1 receptor is the most important adrenergic receptor in the heart so elevated T3 and T4 will increase the number of beta1 receptors there. --> One symptom of hyperthyroidism, the one symptom that usually takes the pts to the doctors is that they are tachycardic and have palpitations. It takes a while to get T3 and T4 under control in hyperthyroidism so during that time, you want to suppress symptoms/effects on the heart and as a result, beta blockers are often given in initial treatment of patients with hyperthyroidism.



- direct adrenergic antagonist
- non-selective beta adrenergic antagonist (beta1 and beta2)
- first generation
- used to treat glaucoma - decreases intraocular pressure by blocking beta2 receptors in the ciliary body in the eye, you can decrease the rate of formation of aqueous humor. Timolol (eye drop) is often used because it doesn't irritate the eye.



- direct adrenergic antagonist
- selective beta1 adrenergic antagonist
- second generation

- can be used cautiously in asthmatics and insulin-dependent diabetics; asthma/diabetes has to be well controlled for at least a year



- direct adrenergic antagonist
- beta blocker with additional actions: alpha1 antagonist
- third generation
- used in pregnancy, does not cause any fetal malformations



- indirect adrenergic antagonist
- depletor: prevents uptake of catecholamines into storage vesicles in sympathetic neuronal varicosities

When norepinephrine is released and taken back up in the cell, in the presence of Reserpine, norepinephrine can't get back inside the storage vesicle and ends up being broken down by MAO. Dopamine too.
After a period of a week or 2, norepinephrine levels will be lowered --> decrease in systolic and diastolic BP

Reserpine problem:
gets into the brain and exerts its action in certain parts of the brain ex) the substantia nigra
Pts taking Reserpine - if storage vesicles in neurons in the SN are depleted, you get a depletion of dopamine --> symptoms of Parkinson's disease

Doesn't cause PD but causes symptoms
Symptoms disappear when you stop reserpine
Not all pts show Sx of PD but there are cases


Botulinum toxin aka Botox

Prevents storage vesicle from fusing with the cell membrane so that the Ach contents cannot be released. Botox has other actions not only in the autonomic NS - if at the neuromuscular junction, botox does the same thing - prevents Ach from being released --> paralyzes the muscle.

Botox is also sometimes used to treat children with cerebral palsy. Cerebral palsy - uncontrolled muscle contractions that make them unable to move/function. Botox is used to cause a partial paralysis in those muscles so that they can't spastically contract --> improves quality of life.


Black widow spider venom

- opposite of botox
- explosive release of Ach (all storage vesicles fuse with membrane, massive concentrations of Ach occur in the autonomic NS and other places like the NMJ)



- direct acting cholinergic agonist
- choline ester (derivatives of Ach)

only used by ophthalmologists in eye-drops to cause constriction of the pupils and accomodation. It is very short-acting. It is not used systemically as a drug because it is hydrolyzed very rapidly by AChE (IV injection of Ach will not last very long, it will very quickly be broken down). It is also not used as drug because it activates nicotinic receptors in addition to muscarinic receptors (don't want to give drug that will cause contraction of muscles and activation of ganglion)



- direct acting cholinergic agonist
- choline ester (derivative of Ach)

an improvement over Ach because it is not broken down by ACE or pseudo-CE, but still a problem because it will activate nicotinic receptors. Carbachol is also only used in the eye when it is used topically as eyedrops. It is used sometimes to treat glaucoma - will cause contraction of the ciliary muscle.



- direct acting cholinergic agonist
- choline ester (derivative of Ach)

not hydrolyzed by cholinesterases, no activity at nicotinic receptors. Number of uses: primarily used to treat paralytic ileus and bladder atony. Paralytic ileus = condition in which parts of the smooth muscle in the small intestine stops contracting or is greatly reduced --> parastalsis disappears or is markedly reduced. This can happen for a variety of reasons - infections in peritoneal cavity, post-abdominal surgery where intestines are manipulated or touched by equipment. Usually temporary - bethanechol is given for 1-2 weeks to jumpstart contractions and after withdrawal, perstalsis is fine. Paralytic ileus can also occur in the very young and the elderly - bethanechol will also jumpstart the contractions in these cases.

Bladder atony - bladder stops functioning. Can see bladder atony under the same circumstances you can see for paralytic ileus - surgery, peritoneal infections, very elderly, very young. Give bethanechol which will jumpstart the bladder.



- direct acting cholinergic agonist
- alkaloid

only has muscarinic activity.
Alkaloids = family of drugs that originally were isolated from plants
Pilocarpine has a few uses: 1. glaucoma - can be applied to the eye topically to cause contraction of the ciliary muscle 2. xerostomia - condition where the patient for a variety of reasons is not producing enough saliva. This is a very serious condition. If untreated, these people lose all their teeth and get big lesions in their mouth. Saliva has components that have anti-bacterial activity in addition to providing lubrication/salivation. Removal = problems.



- AchE inhibitor
- rapidly reversible inhibitor (non-covalent)

drug that positions itself in the active site of AChE and associates with certain aa's in the active site (not the serine hydroxyl group but some other ones). When it sits there, Ach can't bind to the serine hydroxyl group.
Edrophonium = very short lived drug in the body. If given IV, its duration of action is about 15-20 min max. Only one use - help diagnose certain forms of myasthenia gravis (antibodies to cholinergic receptors). MG generally hard to diagnosis - generally try to find Ab but not always detectable. if you give IV edrophonium and see improvement of muscle strength, Edrophonium inhibits AChE for a short period of time, elevated Ach at NMJ, improves grip strength for MG diagnosis.



- AchE inhibitor
- rapidly reversible inhibitor (non-covalent)

used to treat Alzheimer's Disease. Mechanism of action: similar to edrophonium - binds reversibly to certain aa in the active site gorge in the AChE active site. When in there, no Ach can make its way to the serine hydroxyl group.
Only group of drugs approved by the FDA to treat AD
Donepezil has its greatest effect when it's given very early on in the progression of AD although you can still get some effect when the disease is pretty far along. It will slow down the progression of the disease and early on, can reduce some of the symptoms of AD. But not a cure for AD.



- AchE inhibitor
- rapidly reversible inhibitor (covalent)
- carbamate

applied topically to the eye to treat glaucoma. Inhibits AChE in the eye --> accumulation of Ach at the ciliary muscle --> contraction and drainage of aqueous humor from the eye. Not given systemically because it can get into the brain.



- AchE inhibitor
- rapidly reversible inhibitor (covalent)
- carbamate

very similar to physostigmine except neostigmine does not cross the BBB. --> can be given systemically. Used to treat myasthenia gravis (elevates Ach levels at the NMJ) and also often used in combination with Bethanechol to treat paralytic ileus and bladder atony.



- AchE inhibitor
- rapidly reversible inhibitor (covalent)
- carbamate

not a drug but a pesticide that you can buy. They kill pests by inhibiting AChE in those pests --> pests go into cholinergic crisis. Unfortunately, carbaryl and other carbamates in this category will also inhibit human ACE. Each year, there are thousands of people who go into ER in cholinergic crises because they accidentally exposed themselves to large concentrations of pesticides like carbaryl.



- AchE inhibitor
- slowly reversible inhibitor
- organophosphate

drug used for glaucoma. Inhibits AChE in the eye. Popular drug because patients only have to apply it once every 4 days since it's so long lasting. It does not undergo aging --> no permanent inhibition.



- AchE inhibitor
- slowly reversible inhibitor
- organophosphate

not a drug, is a pesticide. You can't buy these pesticides - need license ex) exterminators. Used large scale in agriculture.
2-PAM - an antidote for organophosphate poisoning. 2-PAM = drug that will work faster than the water molecule does - pulls phosphate group off the phosphorylated enzyme intermediate in individuals poisoned with organophosphates.
2-PAM = reactivator. Will not work when aging has occurred. --> anyone with suspected organophosphate poisoning needs to get to ER asap. If the exposure is high enough, patients can show muscle fasciculations, muscle contractions, and muscle convulsions from the inhibition of AChE at the NMJ. You do not use reactivators to treat carbamate poisoning. For some reason, reactivators can actually increase severity of symptoms in carbamate poisoning.



- AchE inhibitor
- slowly reversible inhibitors
- organophosphate

chemical warfare agent aka nerve gases. Act by inhibiting AChE.
Nerve gas vs pesticides or drugs:
1. Nerve gases are very potent inhibitors of AChE - don't need high concentrations of Soman or other nerve gases to be lethal because they're so good at phosphorylating ACE
2. All nerve gases are volatile - designed to be volatile because that is how they are spread. Get into air and either inhale or pass through skin because they're lipid soluble. Pesticides, on the other hand, are non volatile - don't have to worry about breathing them in.
3. Nerve gases will age instantly -as soon as serine hydroxyl group on AChE is phosphorylated, it ages.



- cholinergic antagonist
- natural alkaloid
from gimsen weed, can be lethal if smoked raw (levels of atropine are way too high, gets into the brain and causes hyperthermia)
But it's a good drug and has lots of uses:
Heart - in patient with cardiac emergency, atropine can be used to reduce PNS tone to heart
Eye - primarily used by ophthamologists to block the muscarinic receptors on the constrictor muscle --> atropine will dilate the pupils. Will also affect the ciliary muscle - blocks receptors on ciliary muscle and prevents contraction
Salivary glands - atropine reduces production of saliva, often used for oral surgery (want temporary block of production of saliva)
Respiratory system - atropine causes bronchodilation and reduction in production of mucus. Used to be used for asthma but not anymore, better drugs available now.
Intestines - atropine will reduce peristalsis, can be used as an anti-spasmodic
Bladder - atropine will suppress urination, can be used to treat Urinary Urge Incontinence - often occurs in the elderly: patient is fine but suddenly there is an immediate urge to urinate right away
Cholinergic crisis - atropine is an antidote to SLUD.

In the case of an organophosphate, someone who is poisoned, person will receive 2-PAM and atropine.

In carbamate poisoning, person will only receive atropine.



- cholinergic antagonist

originally isolated from plants. Similar to atropine except Scopolamine also acts in the brain as an anti-emetic (reduces the feeling of nausea/vomiting). Scopalamine is used to treat motion sickness - can be used as patch or oral.


Ipratropium (synthetic quaternary amines)

- cholinergic antagonist
- analog of atropine

Muscarinic blocker used to treat asthma. Used because it is more easily volatilized than the other blockers, can be inhaled much more easily


Benztropine (synthetic tertiary amines)

- cholinergic antagonist

drug used to treat Parkinson's Disease. Blocking muscarinic receptors in certain brain regions in the CNS reduces the symptoms of PD early on in the disease. Mechanism not sure. Helps slow progression and reduce symptoms of PD. But will eventually lose effect and disease will continue to progress.



- ganglionic antagonist

drug that blocks the nicotinic receptors in the sympathetic and parasympathetic ganglia. The effects of mecamylamine can be very complicated - some are predictable and some are not.
1. If you have a tissue like the ciliary muscle in the eye, which only has parasympathetic input. If you block the ganglia on the path of innervation on the PNS that goes to the ciliary muscle, you block the message from getting to the ciliary muscle. No Ach is released to cause the ciliary muscle to contract. In this case, mecamylamine acts like atropine.
2. When you have dual input (both SNS and PNS input into a tissue) and you block both ganglia, effects can be both predictable and nonpredictable.
ex) iris dilator and iris constrictor aka iris sphincter muscles
Under normal conditions, PNS is dominant --> pupils are slightly constricted
If you give mecamylamine, the opposite effect of the NS is dominant --> pupils dilate
Therapeutic effect of Mecamylamine: lowers SBP and DBP
Biggest problem of mecamylamine and what limits its use is its association with orthostatic hypotension.