Intro to ANS Flashcards

1
Q

efferent ANS conduct

A

impulses to heart, smooth muscle and glands

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2
Q

afferent ANS conduct

A

visceral pain stimuli and afferent components of autonomic reflexes.

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3
Q

Sympathetic preganglionic fibers leave CNS through

A

the thoracic and lumbar spinal nerves

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4
Q

Parasympathetic leave CNS through

A

cranial nerves and sacral spinal roots.

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5
Q

effects of stimulation of sympathetic system

A

increase heart rate, blood pressure, mobilize energy stores, increase blood flow to skeletal muscles and heart while diverting flow from skin and internal organs, dilate the pupils and bronchioles.

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6
Q

sympathetic reaction is triggered by

A

direct sympathetic activation of effector organs and by epinephrine released by adrenal medulla

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7
Q

functions of parasmpathetic

A

maintains essential bodily functions like digestiv rpocesses, elimination of waste. balances the sympathetic system. is generally dominant.
-never discharges as a complete system but rather separately

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8
Q

these receive innervation from the sympathetic only

A

adrenal medulla, kidney, pilomotor muscles, sweat glands. (blood pressure is mainly sympathetic as well.

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9
Q

all preganglionic efferent ANS fivers and somatic motor fivers to skeletal muscle release

A

ACH which acts on nicotinic receptors.

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10
Q

all parasympathetic post ganglionic fibers release

A

acetylcholine which acts on muscarinic receptors.

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11
Q

All sympathtic post ganglionic fibers(except sweat glands) release

A

norepinephrine which act on either alpha or beta receptors.

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12
Q

Sweat gland post ganglioinic fivers release

A

ACH on muscarinic receptors.

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13
Q

Dopamine is released by

A

peripheral sympathetic fibers.

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14
Q

Acetylcholine is synthesized

A

in the cytoplasm from acetyl CoA and choline which is catalyzed by ChAT (choline acetyltransferase)

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15
Q

Acetyl CoA is synthesized in

A

the mitochondria

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16
Q

choline is transported from

A

the extracellular fluid into the neuron terminal by sodium dependent carrier (CHT1) (rate limiting step)

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17
Q

ACh is transported from cytoplasm into vesicles by

A

carreir protein on vesicle membrane called vesicular ACh trasnporter (VAChT)

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18
Q

VAChT is an antiporter that

A

couples influx of ACh with an efflux of H+

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19
Q

Release of ACh is dependent on

A

extraceullar calcium and occurs when an on action potential reaches the terminal and triggers sufficient influx of calcium.

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20
Q

AChE splits ACh into

A

choline and acetate

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21
Q

Lipid linked species of AChE are embedded

A

within the post-synaptic membrane and located close to cholinergic receptors ensuring quick inactivation of ACh

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22
Q

aChE is also found

A

in other tissues like red blood cells.

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23
Q

Butyrylcholinesterase(pseudocholinesterase) is found

A

in blood plasma, liver and other tissues.

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24
Q

Tyrosineis transported across

A

the BBB into the adrenergic neuron by System L which is a NA+ independent manner

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25
Q

rate limiting step and the way tyrosine gains entry into the neuron

A

conversion of tyrosine to L-dihydroxypnenylalanine by the enzyme tyrosine hydroxylase.

26
Q

L-DOPA is converted to dopamine by

A

L-aminoaced decarboxylase or DOPA decarboxylase

27
Q

Vesicular monamine transporter(VMAT) translocates

A

dopamine into synaptic vesicles in exchange for H+.

28
Q

in addrenergic neurons, intravesicular dopamine Beta hydroxylase converts

A

dopamine to NE and Ne is stored until release

29
Q

in adrenal medullary cells

A

NEreturns to the cytosol where Phenylethanolamine N methyltransferase (PNMT) converts NE to Epi which is then transported to avesicle for storage.

30
Q

these are released in addition to NE

A

ATP, Dopamine beta hydroxylase and peptide cotransmitters

31
Q

NE and Epi are metabolized by

A

Catechol- O methyltransferase and monoamine oxidase.

32
Q

COMT

A

two forms

  • soluble cytosolic form
  • membrane bound form anchored to RERE-

catalyzes transfer of methyl from S- adenosylmethionine to Oh of catechol.

found in nearly all cells including erythrocytes.

can act on extraneuronal catecholamines

33
Q

mao

A

enzyme located on the outer membrne of mitochondria and expressed on most neurons.

oxidatively daminates monoamines o their corresponding aldehydes, these can be converted in turn by aldehyde dehydrogenase to acids or aldehyde reductase to glycols.

MAO-A preferentially deaminates NE and Epi and srotonin

MAO- B- deaminates dopamine more rapidly than serotonin and NE.

In GI tract plays a protective role preventing acces to the general circulation of ingested indirectly acting amines like tyramine and phenylethylamine.

34
Q

primary mechanism of termination of action of NE that is physiologically released

A

simple diffusion away from the receptor site and reuptake into the nerve terminal or into perisynaptic glia or smooth muscles.

35
Q

Reuptake of NE into nerve terminal

A

happens by Na dependent NE transporter (NET) (Uptake 1

36
Q

Indirectly acting sympathomimetics like tyramine and amphetamines can be taken up into nerve endings useing

A

uptake 1 and displace NE from storage vesicles.

37
Q

Nicotinic receptors

A

on plasma membranes of postganglionic cells, on plasma membranes of muscels innervated by somatic motor fivers. and on membrane of cells in the CNS

38
Q

M1 receptors

A

Gq receptor

found mainly in CNS and autonomic ganglia,

increased cognitive function-CNS
Depolarization- Ganglia

39
Q

M2 receptors

A

Gi receptor

found in heart and presynaptic terminals of peripheral and central neurons. They are INHIBITORY by opening K channells and by inhibiting Ca channels.

responsible for vagal inhibition of the heart
inhibition of ACh and NE release at presynaptic nerve terminals

40
Q

M3 receptors

A

Gq receptor

located in smooth muscle and secreptory glands, mainly excitatory: mediate secretions (salivary, bronchial and sweat) and contraction of visceral smooth muscle.

can also cause relaxation of VASCULAR smooth muscle via release of NO from endothelial cells. the vasculature has M3 receptors but they don’t have innervation by the parasympathetic system. activation leads to rise in intracellular calcium mediated by an increase in IP3. the calcium activates the nitric oxide synthase leading to formation of NO from arginine, NO diffuses into adjacent smooth muscle cells and binds to and activates guanlyl cyclase which makes cGMP from GTP. cGMP dependent protein kinase phosphrylates proteins leading to relaxation and vasodialtion

41
Q

NO synthase

A

found in endothelial cells that line blood vessels

catalyze the formation of NO from arginine

42
Q

potency series for beta adrenergic receptors

A

isoproterenol is more potent then Epi which is more potent than NE

43
Q

Beta 1 receptor

A

Gs receptor

equal affinity for epi and NE

in the her stimulation leads to positive inotropic and chronotropic responses.

NE stimulates renin secretion by direct action on the juxtaglomerular cells of kidney.

44
Q

Beta 2 receptor

A

Gs receptor

higher affininty for Epi than NE

tissues with predominance of Beta 2 (vasculature of skeletal muscle) are very responsive to CIRCULATING Epi released by adrenal medulla.

activates hepatic glycogen phosphyrlase

promotes relaxation of smooth muscle by phosphorylation of myosin light chain kinase to inactive form( bronchial, GI, genitourinary)

in skeletal muscle- increases glycogneoysis and uptake of K

pancrease- increased insulin secretion in beta cells, increased glucagon secretion in alpha cells.

Liver- increased glycogenolysis, increased gluconeogenesis

45
Q

Beta 3 receptor

A

Gs receptor

equal affinity for epi and NE

activates TAG lipase to release free fatty acids.

46
Q

Gs can DIRECTLY enhance

A

the activation of voltage gated Calcium channels in teh plasma membrane of skeletal and cardiac muscles.

47
Q

Beta induces effects( all three receptors

A

actiavtes hepatic glycogen phosphorylase, a rate limiting step in glycogenolysis

Protein kinase A which catalyzes phosphorylation of phosphorylase kinse which activates it and catalyzes inactivation of glycogen synthase. which decreases glycogen synthesis.

48
Q

alpha receptors potency series

A

epinephrine is greater than NE and alot greater than isoproterenol.

49
Q

alpha 1

A

Gq receptor

found on post synaptic membrane of effector organe.

in most smooth muscle- contraction by activation of calmodulin dependent myosin light chain kinase.( vasoconstriction, genitourinary smooth muscle)

In GI- cause hyperpolarization and relaxation by activation of calcium dependent K channels.

In Liver- causes increased glycogenolysis and increased gluconeogenesis

50
Q

Alpha 2

A

Gi receptor

located on presynaptic nerve endings reducing NE release and ACh release

postynaptically on other cells like beta cell of pancrease to reduce insulin release.

with platelets- aggregation
with adipocytes- inhibition of lipolysis

they couple to a variety of effectors.

evoke vasoconstriction by opening voltage gated calcium channels.

51
Q

D1 and D5 receptors

A

Gs receptor

found in brain and effector tissues like smooth muscle and renal vascular bed. causes relaxation of renal vascular smooth muscle

52
Q

D2 receptors

A

Gi receptor found in brain, effector tissues, smooth muscle, presynaptic nerve terminals.

53
Q

D3 receptors

A

Gi receptor found in brain

54
Q

D4 receptor

A

Gi receptor found in brain and CV system.

55
Q

ACh release can be inhibited by

A

ACh acting on presynapatic M2 autoreceptors. and by NE on presynapatic alpha2 receptors.

56
Q

other inhibitory receptors

A

A1, H3 and opioid receptors. even some Beta 2 adrenergic heteroreceptors.

57
Q

NE release can be inhibited by

A

Alpha 2 receptors.

heteroreceptors on sympathetic nerve terminals M2, 5-HT, PGE2, Histamine, Enkephalin, and DA receptors.

58
Q

Enhancement of sympathetic NE release

A

activation of presynaptic Beta 2 adrenergic receptors and angiotensin 2 receptors.

59
Q

NE infusion

A
powerful vasoconstrictor (Alpha 1 effect) it increases Mean arterial pressure.
if baroreceptors not in tact it will increase heart rate and contractile forces by beta 1 effect

if baroreceptors intact, there will be negative feedback when MAP is increased which will cause a decrease in sympathetic flow in the heart which will mean an increase in parasympathetic discharge on the pacemaker resulting in bradycardia. which is OPPOsiTE of NE direct action.

60
Q

eye-alpha 1 receptor

A

pupillary dilator muscle in the iris

when active it will cause contraction of dilator- mydriasis

61
Q

eye - M3 receptor

A

pupillary constrictor, ciliary muscle

will cause constriction of iris- miosis
will cause contraction of ciliary muscle (cyclospasm if marked contraction) so that it can focus at short range.. when it relaxes it will cause long range focus .
- this also causes aqueous humor to flow into canal of schlemm which reduces intraocular pressure.

62
Q

eye-beta 2 receptor

A

secretory epithelium of ciliary body

causes secretion of ciliary epithelium that produces aqueous humour.