Intro to ANS

Question 1

efferent ANS conduct

Answer 1

impulses to heart, smooth muscle and glands

Question 2

afferent ANS conduct

Answer 2

visceral pain stimuli and afferent components of autonomic reflexes.

Question 3

Sympathetic preganglionic fibers leave CNS through

Answer 3

the thoracic and lumbar spinal nerves

Question 4

Parasympathetic leave CNS through

Answer 4

cranial nerves and sacral spinal roots.

Question 5

effects of stimulation of sympathetic system

Answer 5

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.

Question 6

sympathetic reaction is triggered by

Answer 6

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

Question 7

functions of parasmpathetic

Answer 7

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

Question 8

these receive innervation from the sympathetic only

Answer 8

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

Question 9

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

Answer 9

ACH which acts on nicotinic receptors.

Question 10

all parasympathetic post ganglionic fibers release

Answer 10

acetylcholine which acts on muscarinic receptors.

Question 11

All sympathtic post ganglionic fibers(except sweat glands) release

Answer 11

norepinephrine which act on either alpha or beta receptors.

Question 12

Sweat gland post ganglioinic fivers release

Answer 12

ACH on muscarinic receptors.

Question 13

Dopamine is released by

Answer 13

peripheral sympathetic fibers.

Question 14

Acetylcholine is synthesized

Answer 14

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

Question 15

Acetyl CoA is synthesized in

Answer 15

the mitochondria

Question 16

choline is transported from

Answer 16

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

Question 17

ACh is transported from cytoplasm into vesicles by

Answer 17

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

Question 18

VAChT is an antiporter that

Answer 18

couples influx of ACh with an efflux of H+

Question 19

Release of ACh is dependent on

Answer 19

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

Question 20

AChE splits ACh into

Answer 20

choline and acetate

Question 21

Lipid linked species of AChE are embedded

Answer 21

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

Question 22

aChE is also found

Answer 22

in other tissues like red blood cells.

Question 23

Butyrylcholinesterase(pseudocholinesterase) is found

Answer 23

in blood plasma, liver and other tissues.

Question 24

Tyrosineis transported across

Answer 24

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

Question 25

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

Answer 25

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

Question 26

L-DOPA is converted to dopamine by

Answer 26

L-aminoaced decarboxylase or DOPA decarboxylase

Question 27

Vesicular monamine transporter(VMAT) translocates

Answer 27

dopamine into synaptic vesicles in exchange for H+.

Question 28

in addrenergic neurons, intravesicular dopamine Beta hydroxylase converts

Answer 28

dopamine to NE and Ne is stored until release

Question 29

in adrenal medullary cells

Answer 29

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

Question 30

these are released in addition to NE

Answer 30

ATP, Dopamine beta hydroxylase and peptide cotransmitters

Question 31

NE and Epi are metabolized by

Answer 31

Catechol- O methyltransferase and monoamine oxidase.

Question 32

COMT

Answer 32

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

Question 33

mao

Answer 33

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.

Question 34

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

Answer 34

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

Question 35

Reuptake of NE into nerve terminal

Answer 35

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

Question 36

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

Answer 36

uptake 1 and displace NE from storage vesicles.

Question 37

Nicotinic receptors

Answer 37

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

Question 38

M1 receptors

Answer 38

Gq receptor found mainly in CNS and autonomic ganglia, increased cognitive function-CNS Depolarization- Ganglia

Question 39

M2 receptors

Answer 39

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

Question 40

M3 receptors

Answer 40

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

Question 41

NO synthase

Answer 41

found in endothelial cells that line blood vessels | catalyze the formation of NO from arginine

Question 42

potency series for beta adrenergic receptors

Answer 42

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

Question 43

Beta 1 receptor

Answer 43

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.

Question 44

Beta 2 receptor

Answer 44

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

Question 45

Beta 3 receptor

Answer 45

Gs receptor equal affinity for epi and NE activates TAG lipase to release free fatty acids.

Question 46

Gs can DIRECTLY enhance

Answer 46

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

Question 47

Beta induces effects( all three receptors

Answer 47

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.

Question 48

alpha receptors potency series

Answer 48

epinephrine is greater than NE and alot greater than isoproterenol.

Question 49

alpha 1

Answer 49

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

Question 50

Alpha 2

Answer 50

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.

Question 51

D1 and D5 receptors

Answer 51

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

Question 52

D2 receptors

Answer 52

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

Question 53

D3 receptors

Answer 53

Gi receptor found in brain

Question 54

D4 receptor

Answer 54

Gi receptor found in brain and CV system.

Question 55

ACh release can be inhibited by

Answer 55

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

Question 56

other inhibitory receptors

Answer 56

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

Question 57

NE release can be inhibited by

Answer 57

Alpha 2 receptors. heteroreceptors on sympathetic nerve terminals M2, 5-HT, PGE2, Histamine, Enkephalin, and DA receptors.

Question 58

Enhancement of sympathetic NE release

Answer 58

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

Question 59

NE infusion

Answer 59

``` 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.

Question 60

eye-alpha 1 receptor

Answer 60

pupillary dilator muscle in the iris when active it will cause contraction of dilator- mydriasis

Question 61

eye - M3 receptor

Answer 61

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.

Question 62

eye-beta 2 receptor

Answer 62

secretory epithelium of ciliary body causes secretion of ciliary epithelium that produces aqueous humour.