This post actually has nothing to do with the church/ dogma, etc...
I have a midterm tomorrow worth almost half of my course grade in pharmacology and I need some help with drugs ???
Atropine and Hexamethonium are both cholinergic blockers (or so it seems from my notes) so why is it that Hexamethonium makes the sympathetic to be parasympathomimetic and vice versa, while atropine only seems to block the parasympathetic effects?
This is very confusing, so if anyone could clear this up for me, that would be great!
Thank you... God Bless!
Here's the full description at wikipedia: h t t p://en.wikipedia.org/wiki/Hexamethonium (remove the space between h t t p)
Mina, Thank you for offering to help! I know you've asked me to im you but, if it's not too much trouble can I ask you to explain it here or via a pm? I just don't feel comfortable adding people I don't know
Thank you so much!
ps. are you a pharmacist?
Also while you’re here :) I just wanted to clarify one more thing: muscarinic agonists work in the same way as choline esters (ie. Ach, bethanecol, and carbachol) and they’re all parasympathomimetic... but muscarinic agonists release EDRF so does that mean they only work on blood vessels?
lol can’t wait to be a pharmacist in training!!
EDRF is a diffent catgory then ACH and musuarinic againsts or anything.. the release of EDRF is a result PSNS activation of the endothelial cells iun the blood vessels. those EDRF have othere checmials like NO that dilate the vessels..
belive me.. u wount wanna b when u are lol =p
I hope that helps.
btw... I haven't finished studying yet and I might have some more questions. If you leave, will you be on later tonight??
ie. I have pilocarpine, pirenzipine, and phentolamine that all end in "-ine" but do completely different things and I can never remember which one is which unless I look at the notes!
Any tips from the expert?
First, you have to understand what each receptor does before understanding how each drug acts
There are 3 types of cholinergic receptors
1-Nicotinic(N) receptors which act the neuro junctions and these are primarily activiated by nicotine (Nicotine is the agonist), and also activated by sympathetic agonists (Epinephrine)
2- Nicotinic (M) receptors which act at the skeletal muscle junctions and these are also activated by Nicotine
3- Muscarinic receptors which act at the effector sites (glands, heart, GI, etc) and these are activated by muscarine
Also you need to understand what a sympathomimitic/lytic means
Mimitics comes from the word mimic, so sympathomimitic mimic or activates the sympathetic nervous system
Lytics come from the word lyses, so sympatholytics blocks the activity of sympathetic nervous system
So back to your question, yes Atropine and Hexamethonium are both cholinergic blockers, but they don’t have the same actions
Hexamthonium only blocks the Nicotinic (N) receptors , so as a result blocks the action of both Nicotine and Epinephrine resulting in blocking both the sympathetic and the parasympathetic nervous systems at once, thus why it’s called a “Sympatholytic”, and “Parasympatholytic”
But, Atropine only acts at the Muscarinic receptors, resulting in a block of the parasympathetic nervous system, that’s why it’s called “parasympatholytic”
Sorry I don’t have any advice on how to remember the drug names, you just have to memorize it.
Hope that helps
Another couple questions:
1. How does the inhibition of adenylyl cyclase and cAMP by alpha 2 agonists reduce hypertension. I know that alpha 2 works in the heart better than alpha 1 and that beta 1 is the most significant receptor in the heart. I also know that the heart is mainly under parasympathetic tone, which prevents it from beating too fast... I just can't put all the pieces together!
2. How can alpha agonists and alpha blockers both be antihypertensives? Is it because the agonist has a direct effect, while the antagonist allows for more receptors to be hypersensitive so it's more indirect?
First you have to know what Epinephrine does. Epinephrine is a hormone which acts as a vasoconstrictor , and activates the fight and flight mechanism. So increased amounts of epinephrine leads to increased in blood pressure
Alpha 2 agonist (Centrally acting hypertensive, ex: Clonidine)
It acts in the central nervous system, It binds to alpha 2 receptor in the presynaptic cell in the neuron, and it activates the receptor, leading the cell to –ve feedback to the cell (making it think that it produces too much epinephrine) which leads to decreasing the amounts of Epinephrine produced leading to decreased epi levels in the body, leading to decreased blood pressure.
Alpha 1 antagonist (peripherally acting, ex: Doxazosin, Prazosin)
When activating alpha 1 receptors in the body (ex: blood vessels), this leads to increases vascular resistance, and increase blood pressure
The amount of Epinephrine in the body stays the same, but it can’t bind to the alpha 1 receptors which causes vasoconstriction.
So alpha 1 antagonist replace the binding of Epinephrine, causing vasorelaxation, and reduced blood pressure
Beta receptors (three types)
Beta 1 is mainly found in the hearts and is regulated by both Sympathetic (Epinephrine), and parasympathetic (Acetylcholine),
When Epinephrine activates B1 receptor, the heart beats faster (tachycardia) due to sympathetic system, when acetylcholine activates B1 receptor, the hearts beats slower (bradycardia), due to parasympathetic nervous system.
You can think of both the sympathetic and parasympathetic nervous system as two opposite systems that keep the body in check.
Hope that helps
Good Luck on your exam
Epinephrine will bind to the alpha 1 receptor in case there is too much Epinephrine circulating around, so it binds to the receptor to provides -ve feedback (it tells the receptor, Hey, there's too much of me here, tell the cell not to make anymore)
So when the drug binds (Alpha 1 agonist), it acts like Epinephrine, and provides the same -ve feedback, and reduces Epinephrine production (lies to the cell, and says there's too much Epinephrine around here, don't make anymore, even though there is little amount of Epinephrine).
So in that case Epinephrine isn't produced as much, and there's less vasoconstriction, low bp, etc...
Does that make sense?
Hope it does :)
please pray for me tomorrow... I'm so worried that I won't be able to remember all these drugs!!! you're a pharmacist so you probably know what it's like...
I need all the prayers I can get!
thanks Marmoura99 for initiating a nonreligious topic.I know this forum is full of experts in many fields.I am also in trouble with my course.If I may ask the experts;how come a mosquito is not capable of transmitting the HIV virus,while it can transmit other disease carrying viruses such as the west nile virus that is prevalent in the eastern part of the USA?I can not find relevant information on this one. Please,if anyone knows a good explanation,I am thankful.Important exam next week(thursday).Marmoura,hopefully your exam went well.
sodr i agree... i dotnt wanna go to college anymore!
Yeah, but are you going to study pharmacy and have to learn all this stuff?
what a relief ! haha
I do not know exactly what you study or if you will have to do a lot with drugs (in the pharmacological sense,of course;-).
I just want to recommend you a great book.
Pharmacology: Rang and Dale
It is easily written.You do not need to buy it,every library has it. The, you will not have to rely on them professional pill counters in the future.
Its Pharmacology, 6th Edition, Rang/Dale/Ritter/Flower .. Churchill Livingstone Elsevier 2007...
and another one, if u havent already heard of, is..
Drug Discovery and Development, Rang/Dale/Ritter/Flower .. Churchill Livingstone Elsevier , 2006
Take Care and God Bless.