Epinephrine Norepinephrine Isoproterenol

[Doc Ivy]

Does anyone care to wax philosophically on the CO, HR, BP changes related to these drugs?

for example if NE is selective for BOTH a1 and a2 why does it cause and increase in MAP? is it because of the B1 effect on the heart?
Why does epi not cause a change in MAP, is it due to the receptor distribution of a1 versus B2?


do you look at BP first and then try to figure out what the HR response will be?
is MAP what determines the HR baroreceptor response, or is is systolic or diastolic BP?
is CO the main determinant of systolic BP? Is TPR the main determinant of diastolic BP? or am I just making things up?

Anyone can jump in with more questions or answers.

Thanks

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[streetdoc]

i'll add that not all receptors are created equal. if i'm remembering correctly, NE has very little a2. and remember that you're going to get a dose variety too. beta are stim first therefore it's a lot like isopro...
and i always loved the epi reversal with the a1 blocker...i love pharm

 

[omarsaleh66]

NE will give u High MAP in addition to other symtoms cuz it hits a1 harder than others

Epi hits Beta 2 more than NE so u get more relaxation of the arteries but not as much as Isoproternol cuz there is still some alpha agonism here too.

Isoproterenol is only Beta1,2 agonist so here u will see an increased heart rate and at the same time, u will get the most relaxation of the arteries cuz no alpha agonism. So this drug gives the largest drop in MAP of the 3 agents.

THis is from a question I did in A&L so its fresh in my memory, gluck!!

 

[Doc Ivy]

Thanks, that B2 getting hit first is ringing a bell--- I love the a1 Epi reversal too

Thanks guys

 

[HiddenTruth]

Omar pretty much said it all. But what's wierd is that with NE, the reflex is BRADY, despite the increased B! effect, so the alpha 1 effect is more prominent than the B1, and so you will get increase in BP, and CO, and intially an incrs in HR, but later on you get bradycard, because of the reflex from the strong alpha1agonistic response. If you're doing this from kaplan pharm, some of those tracings are maad hard and really wierd (like one of them they show that AcH can cause reflex tachy, which is really wierd--i don't really believe that-- =).

But, yea think of epi in terms of other drugs; at low doses it acts like isopro, and at high doses, the tracings look just like NE. But, the important thing of epi is that it has minimal to none b2 activity, and that is why when u give alpha blocker, u get huge drop in BP (unopposed B2 activity, where as in NE u won't get that drop). Alrite, I think im just blabbing now, u guys know all this. This stuff is cool.

P.S: good to see u back on the forum, A.

 

[streetdoc]

Omar pretty much said it all. But what's wierd is that with NE, the reflex is BRADY, despite the increased B! effect, so the alpha 1 effect is more prominent than the B1, and so you will get increase in BP, and CO, and intially an incrs in HR, but later on you get bradycard, because of the reflex from the strong alpha1agonistic response. If you're doing this from kaplan pharm, some of those tracings are maad hard and really wierd (like one of them they show that AcH can cause reflex tachy, which is really wierd--i don't really believe that-- =).

I may be able to shed light on the Ach reflex tach thing...
ok, my thinking is this. vessels have some M (i believe M3) receptors on them that work thru NO. so, if you you give an M agonist (Ach), then you will see relaxation of vessels and then you get your tachy.
that was actually on our pharm final. our prof is the kaplan pharm man and if he puts it on the test, you better know it for step 1.
i hope that helps...if i'm way wrong let me know that too!
streetdoc

 

[Doc Ivy]

Yes, I think I remember this point too... when you give Ach iv, you'll see the vascular effects first-- Nitric oxide mediated vasodilation leading to reflex tachy--- you'll really only see a direct Brady effect of Ach if you give it intracardiac or in such a huge dose that can actually get to the heart

 

[HiddenTruth]

I may be able to shed light on the Ach reflex tach thing...
ok, my thinking is this. vessels have some M (i believe M3) receptors on them that work thru NO. so, if you you give an M agonist (Ach), then you will see relaxation of vessels and then you get your tachy.
that was actually on our pharm final. our prof is the kaplan pharm man and if he puts it on the test, you better know it for step 1.
i hope that helps...if i'm way wrong let me know that too!
streetdoc[/QUOTE]

a ha--makes sense, nice work. Yea, so I suppose any of the effectors mediated thru NO can do this, like hist, 5HT, Ach, NO.

Does anyone understand glaucoma well? Like, open vs. closed and all the various tx u can give. I don't really understand this--will appreciate the input.

 

[caribsun]

But, yea think of epi in terms of other drugs; at low doses it acts like isopro, and at high doses, the tracings look just like NE. But, the important thing of epi is that it has minimal to none b2 activity, and that is why when u give alpha blocker, u get huge drop in BP (unopposed B2 activity, where as in NE u won't get that drop). Alrite, I think im just blabbing now, u guys know all this. This stuff is cool.

P.S: good to see u back on the forum, A.

why dont u get BP drop with alpha blocker with NE?

 

[streetdoc]

why dont u get BP drop with alpha blocker with NE?

NE does not have B2!
when you give an A1 blocker in EPI, you "unmask" the B2 action. therefore "the drop" is seen in BP

 

[Doc Ivy]

Hey Hidden, I'll try to shed some light on the glaucoma story:

basically mydriasis of the pupil tends to crowd the angle between the cornea and the iris thereby exacerbating narrow angle glaucoma-- when the angle is too acute aqueous humor can't get out of the canal of schlemm and it the intraocular pressure goes up. That's why a pt with narrow angle glaucoma complains after being in a dark room, cuz their pupils dilate and it hurts. Constricting the pupil decrowds the angle so that aqueous humor can flow more easily. So you treat closed/narrow angle glaucoma with things like timolol (beta blocker-- decrease sympathetic= less mydrasis) or with cholinergics/ anticholinesterases which promote miosis like carbachol, physostigmine, and tropicamide

as far as open angle glaucoma goes I think acetazolamide is the tx of choice just to reduce the amount of humor produced
hope it helps.

 

[streetdoc]

Hey Hidden, I'll try to shed some light on the glaucoma story:

basically mydriasis of the pupil tends to crowd the angle between the cornea and the iris thereby exacerbating narrow angle glaucoma-- when the angle is too acute aqueous humor can't get out of the canal of schlemm and it the intraocular pressure goes up. That's why a pt with narrow angle glaucoma complains after being in a dark room, cuz their pupils dilate and it hurts. Constricting the pupil decrowds the angle so that aqueous humor can flow more easily. So you treat closed/narrow angle glaucoma with things like timolol (beta blocker-- decrease sympathetic= less mydrasis) or with cholinergics/ anticholinesterases which promote miosis like carbachol, physostigmine, and tropicamide

one itty bitty point (that my pharm prof mantioned) is that Beta blockers --and the CA inhibs--decrease the production...THC does too i believe and a few more things. anyway, beta blockers may lead to less mydriasis, but they mainly decrease production as far as ai know

streetdoc-
pharm lover

 

[Pox in a box]

I'd love to comment on this...next week. See you then.

 

[caribsun]

NE does not have B2!
when you give an A1 blocker in EPI, you "unmask" the B2 action. therefore "the drop" is seen in BP

NE has B2, it's just less sensitive than E

 

[HiddenTruth]

NE has B2, it's just less sensitive than E

true but this is a significant diffr, and as far as the exam is concerned, i think iNE would only have activ with a1, a2, and b1--if u look at the tracings, the classic way to differentialte btwn epi and norepi is to give the alpha blocker, and u get a drastic drop in BP with epi, but not with NE, because the B1 kicks in, and there is none to minimium unopposed b2 activ with NE.