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49 Cards in this Set

  • Front
  • Back
Different btwn pre-GN and GN fibers
Pre-GN are myelinated and post-GN are not
SNS and PS difference
Other than function, SNS preGN to GN cell ratio is 1:20 with extensive overlap, while PS is 1:1
Botuline does what
inhibits vesicle fusion and hence no release of ACh
What inhibits Choline uptake
Mechanism of alpha 1
via Gq
Mech of alpha 2
Mech of beta 1, beta 2 and D 1
Gs via increase AC and cAMP
What blocks uptake of Dopamine into vesicle inorder to make NE
What causes lipolysis in the fat cells
SNS through beta 1 receptor
beta 2 and D1
glycogenalysis receptors
alpha 1 and beta 2, beta being dominant one (in liver and muscle)
Epi action on vessels
low dose: beta 2 are more sensitive than alpha one, so causes vasodilation
High Dose: alpha 1 predominates, causing vasoconstriction
NE action's on which receptors?
alpha 1 and 2, and beta 1. Not much on beta 2
Isoproterenol action's on which receptors?
beta 1 and beta 2 with little effect on alpha receptors... resulting in low BP
How is Isoproterenol different than EPI?
less hyperglycemia compared to EPI
Dopamine effect's on what receptor?
Low Dose: D1 in kidney, Beta 1 in heart
High Dose: stimulate alpha receptors

Overall: high HR, High MCF, High CO
Dobutamine effect's which receptors?
Beta 1 only resulting in higher MCF and HR

Less stimulation of HR than ISOP... so less arrhythmias than EPI, ISOP and DA

Overall: little effect on BP... just increase in contractility (better in a sick heart).
compare EPI and NE
EPI activates all receptors, resulting in overall decrease in TPR, with increase in Systolic and decrease in diastolic pressure.

NE causes overall increase in TPR as no beta 2 receptors are activated. both syst. and diastolic go up.
Dopamine receptor dose effect
going from low dose to high; D > beta > alpha.
Bulky structure of a sympathomimetic amines does what?
makes it more beta agonistic
removal of OH group from catechol does what?
makes it more CNS penetrative
What's the significant of catechol group as far as breaking it down?
these are needed so that the OH group can be methylated by COMT. So, ephedrine, phenylephrine, amphetamine etc are not broken down by COMT givig them increase half life and greater action.
Amphetamine action?
release NE from nerve terminal by displacing it

direct effect on alpha and beta just like NE action.

CNS effects:
Ephedrine and pseudoephedrine action
release NE from nerve terminal

directly stimulate beta 2 receptors. less CNS action than amphetamine
What are the agents that displace stored catecholamines?
amphetamine and ephedrine and pseudoephedrine
agents that inhibit uptake of released catecholamine?
cocain, tricyclic antidepressants (imipramine), antiobesity drugs (sibutramine).
cocaine action?
local anestheic, prevents uptake of NE by inhibiting the NE transporter... has CNS activity
MAO inhibitors action?
includes phenelzine... treat depression. can result in increased Tyramine due to lack of its breakdown leading to palpitations, headache and hypertensive crisis
all about phenylephrine
alpha 1, alpha 2 agonist (1 > 2)
beta 2 agonist, cause less cardiac stimulation
D1 agonist, lows BP, IV admin. for short term severe hypertension.

DA itself on the other hand increase BP b/c of its effects on beta and alpha receptors as well.
What are irreversible alpha receptor blockers? function?
phenoxybenzamine: decrease TPR and BP, reflex increase in HR and CO.

binds alpha receptors covalently.

Sharp drop in MBP in hypovolumic inviduals.
non selective reversible alpha blocker?
phentolamine: blocks a1 and a2... decreased TPR, and reflex cardiac stimulation.
alpha 1 selective blocker?
Prazosin: most widely used class of antagonists

less reflex tachycardia and greater antihypertensive efficacy.
Therapeutic uses of alpha receptor antagonists?
hypertension, pheochromocytoma, BPH, erectile dysfunction
Side effects of alpha antagonists?
postural hypotensions, nasal stuffiness, reflex cardiac stimulation, impaired ejaculation.
How is HR increased in non-selective alpha antagonists?
When alpha 2 is blocked, more NE is released, causing increased HR.
beta 1 selective blocker?
atenolol with just blocking b1, you aren't causing bronchoconstriction... good for people with asthma!

large dose of selective blockers become non-selective.
beta blocker with partial agonist activity?
pindolol is b1 and b2 clocker with ISA. Causes less slowing of HR at rest than those without ISA.
non selective beta blocker?
What are the effects of propranolol?
Cardiac: decrease HR, MCF, CO, conduction vel., O2 demand, automaticity

Vascular: increased TPR, causing decrease renin [in hypertensive pts, a net effect of delayed drop in BP]
What are the metabolic effects of propranolol?
increased VLDL and decrease HDL

slows recovery of glc levels after insulin admin. in diabetics.
What are the bronchioles effects of propranolol?
indications for beta blockers?
hypertension, ischemic heart dz (angina, post MI), arrhythmias, CHF, open angle glaucoma, prophylaxis for migraine headaches, termor (performance anxiety)
contraindications for beta blockers
bronchoconstriction, bradycardia, av block, cardiac arrest and failure,

Sudden withdrawal may cause angina, MI, elevated BP

excercebation of insulin-induced hypoglycemia, and maksing reflex tachcardia,

increased VLDL, decrease performance, sedation, depression
what are some mixed antagonists?
labetalol, carvedilol
labetalol actions?
sel. alpha 1 and non-selective beta blocker (1:3 ratio oral, 1:7 following IV)
What are some uses of labetalol
so alpha 1 and beta 1, 2 blocker

hypertension, pheochroocytoma induced HTN, angina pectoris
What are some adrenergic neuron blockers?
guanethidine: takes the NE transporter into the nerve end, preventing release of NE. No effect on adr. medulla, or BBB crossing