PDA cluster 1 part 2
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Created by:
ccuteandsporty09 on February 1, 2012
Subjects:
Principles of Drug Action Intro
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34 terms
Terms | Definitions |
|---|---|
 What are the 3 factors that control blood pressure? | blood volume, heart rate, and vascular resistance or tone |
| Make up of blood vessels2 | inner endothelial layer, then smooth muscle layer which determines the resistance by dilation or constriction |
| smooth muscle3 | sympa, NE, A1 |
| An increase in firing frequency in sympa effects BP how? | increase |
| A decrease in firing frequency in sympa effects BP how? | decrease |
| What happens to the mean BP when parasympathetic activity is increased?2 | it decreases, but there aren't alot of parasympathetic innervation of blood vessels so this is a secondary consequence of inhibiting HR |
| parasympatetic control of vasomotor tone (blood vessels) | localized |
| Sympathetic effect on the heart5 | B1, NE, increase HR at the SA node, increase force of contraction by making cardiac muscle more receptive to AV impulses, increase conductivity |
| Parasympathetic effect on the heart5 | M2, Ach, decrease force by acting on cardiac muscle, decrease HR at SA node, decrease conductivity at AV node |
| Path of impulses in heart3 | SA, AV, muscle |
| At rest the primary determinant of HR (less than 100) is? | parasympathetic |
| At activity the primary determinant of HR (more than 100) is? | sympathetic |
| baroreceptors, where and what does increased firing mean4 | afferent neurons that measure BP, 3, aortic arch and carotid vessels, increased firing increases BP |
| Afferents from the baroreceptors terminate where | NTS in medulla |
| NTS2 | inhibit sympathetic neurons and stimulate vagal nerve |
| vagal nerve | part of the parasympathetic pathway the releases Ach at the heart |
| at blood vessels NTS2 | decreases sympathetic tone, dilation |
| the more baroreceptors fire2 | increase NTS, decrease HR |
| neuropathic postural tachycardia2 | HR goes up when they stand up because blood vessels restrict but baroreceptors don't fire, increased sympa activity even though you have elevated BP |
| Ach does what to the SA node | decreases firing |
| Adrenal medulla/gland4 | 2 tissues fused together, exclusively sympathetic, inner is medulla outer is cortex, medulla get Ach and release Epi and NE |
| Pheochromocytoma2 | tumor in medulla causing increased release of Epi and NE, tachycardia and high BP |
| Adrenergic/sympathetic transmission8 | tyrosine to tyrosine hydroxylase, to DOPA, to dopamine, to VMAT vesicles, to NE, depolarization of the nerve, reacts with A and B receptors, also acts at nerve terminal and auto receptors |
| Depolarization of nerve in adrenergic transmission5 | inside of cell is negative (-80mV), action potential comes down the axon and Na channels open up causing inside to become positive (40mV), Ca channels open up with positiveness, Ca triggers fusion of vesicle and plasma membrane, neurtransmitter is released |
| Ca channels | voltage gated |
| How do you turn the adrenergic transmission off?2 | wash out NE and it diffuses away from site of activity, most of it is taken back up by a transporter |
| autoreceptors5 | on the presynaptic membrane that responds to the same transmitter that is released by that terminal, feedback, regulates amount of transmitter released, block synthesis of neurotransmitter, activate tranporter so uptake is faster |
| The transporter for NE is a target for what and what does this mean?2 | cocaine and meth, they block the transporter from taking up NE |
| metyrosine2 | acts on tyrosine hydroxylase, used for phenochromocytoma |
| reserpine3 | hypertensive, inhibits VMAT, can't get NE into vesicles |
| cholinergic neurotransmission | process is the same except with acetylcholine |
| how do you turn off cholinergic neurotransmission | acetylcholinesterases break down acetylcholine into choline and acetate |
| acetylcholinesterase inhibitors | Ach is not broken down |
| botulum toxin2 | Ach cannot fuse with membrane, can cause paralysis because it effects skeletal muscle |
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