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79 Cards in this Set
- Front
- Back
Parasympathetic Ganglion:
Neurotransmitter, Receptor, Receptor Dynamic |
NT: ACh
Receptor: Nicotinic Receptor: 80 Å pentemeric Sodium Channel, Requires both Alpha sites bound to open (for milliseconds) Pharm-ASN-h-2 Pharm-Pharmacodynamics-h-5 |
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Which sacral roots cary PSNS fiber?
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The third and fourth roots
Pharm-ANS-h-2 |
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Parasympathetic Synapse at Target:
Neurotransmitter, Receptor, Receptor Dynamic |
NT: ACh
Receptor: Muscarinic M2: Gi decrease cAMP M1 & M3: Gq, increase IP3/DAG Pharm-ANS-h-2 Pharm-Phdynam-h-8 Pharm-ANS-h-2 |
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coordinated discharge
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the simultaneous interaction of several SNS neurons, possible because the paravertebral chains have broad interconnections
Pharm-ANS-h-2 |
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NT of the postganglionic SNS neurons
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Most: NE
Sweat Glands: ACh Renal Vasculature: Dopamine |
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Sympathetic Ganglion:
Neurotransmitter, Receptor, Receptor Dynamic |
NT: ACh
Receptor: Nicotinic Receptor: 80 Å pentemeric Sodium Channel, Requires both Alpha sites bound to open (for milliseconds) Rapidly desensitized Pharm-ASN-h-2 Pharm-Pharmacodynamics-h-5 |
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SNS Adrenal innervation
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preganglionic fibers release ACh, postganglionic cells release E directly into the blood stream.
Pharm-ANS-2 |
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In what circumstances does ACh act on nicotinic receptors?
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BOTH SNS & PSNS pre-ganglionic fibers
SNS to the adrenal medulla (causing the release of epinephrine) motor neurons to Skm. Pharm-ANS-h-3 |
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In what circumstances does ACh act on muscarinic receptors?
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post-ganglionic fibers of the parasympathetic system
sweat glands, even though these neurons are considered sympathetic Pharm-ANS-h-3 |
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From what cells is NE released?
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Post-ganglionic SNS
Pharm-ANS-h-3 |
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In what PNS scenario is Dopamine released
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SNS to renal vasculature smooth muscle
Pharm-ANS-h-3 |
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myenteric plexus
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Auerbach’s plexus
part of ENS which controls contraction and relaxation Pharm-ANS-h-3 |
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submucosal plexus
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Meissner's plexus
part of ENS which controls secretions, absorption, and blood flow Pharm-ANS-h-3 |
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vagal inputs to the ENS
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excitatory, modulatory
ACh causes stimulation of smooth muscle in the GI tract, and also increases secretion of mucosa and gastric acid Pharm-ANS-h-3 |
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sympathetic to the ENS
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inhibitory, modulatory
NE and E inhibit GI activity and dcrease ACh release Pharm-ANS-h-3 |
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Serotonin in the ENS
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the major intrinsic excititory NT
Pharm-ANS-h-3 |
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NO in the ENS
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the major intrinsic inhibitory NT
Pharm-ANS-h-3 |
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VIP in the ENS
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minor inhibition of GI activity
Pharm-ANS-h-3 |
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vasoactive intestinal peptide in the ENS
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acts on PY2 receptors:
minor inhibition of GI activity Pharm-ANS-h-3 |
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substance P in the ENS
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with neurokinin A, released in combination with ACh, excititory
Pharm-ANS-h-3 |
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neurokinin A in the ENS
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with substance P, released in combination with ACh, excititory
Pharm-ANS-h-3 |
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ATP in the ENS
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Acts on P2X purinergic receptors
exvitatory Pharm-ANS-h-3 |
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ChAT
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choline acetyltransferase
syntesizes ACh from choline and acetyl CoA. Pharm-ANS-h-4 |
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VAT
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Vesicle ACh Tranporter
Transports ACh into storage vesicles. Can be blocked by Rx vesamicol Pharm-ANS-h-4 |
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Vesamicol
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Rx: blocks VAT (Vesicle ACh Tranporter) from moving ACh into presynaptic vesicles
Pharm-ANS-h-4 |
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VAMPs
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Vesicle Associated Membrane Proteins- align the pre-synaptic veslces with SNAPs at release sites.
Includes: v-SNARES of ACh exocytosis can be digested via serine protease botulinum toxin Pharm-ANS-h-4 |
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SNAPs
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synaptosomal nerve-associated proteins
proteins on inner leaflet of outer membrane in charge of exocytosis includes: t-SNARES of ACh exocytosis can be digested via serine protease botulinum toxin Pharm-ANS-h-4 |
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botulinum toxin
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AB exotoxin, serine protease
digests t-SNARE and v-SNAREs, prevents ACh vesicle release Pharm-ANS-h-4 |
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acetylcholinesterase
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present in Cholinurgic synaptic clefts, & in RBC's,
pseudo AChE in other ts. Non-Synaptic AChE's involved in some Rx metabolism Pharm-ANS-h-5 |
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hemicholinium
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Rx used to block high affinity transporter of Choline back into the presynaptic varicosoty
Pharm-ANS-h-5 |
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Mobile Pool of NE
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a pool of free NE in the nerve terminal in addition to NE stored in vesicles
Pharm-ANS-h-5 |
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Catecholamine Prodxn
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Na+/Tyrsine cotransport into cell
Tyrosine Hydroxylase creates L-Dopa (RLS, Blocked by Rx metyrosine, upregulated during SNS dominance) L-Dopa decarboxylated to DA DA hydroxylated to NE NE converted to E Pharm-ANS-h-5 |
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Tyrosine Hydroxylase
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Converts Tyrosine to L-Dopa
This is the Rate Limiting Step in Catecholamine Synthesis Blocked by Rx Metyrosine Both activity and gene expression upregulated with SNS activity. Pharm-ANS-h-5 |
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Metyrosine
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Rx blocks Tyrosine Hydroxylase
TH is he Rate Limiting Step in Catecholamine Synthesis, converts Tyrosine to L-Dopa Pharm-ANS-h-5 |
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VMAT
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Vesicular Monoamine Transporter
Moves Catecholamines into vesicles. May be blocked with Rx reserpine Pharm-ANS-h-5 |
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Reserpine
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Blocks
Vesicular Monoamine Transporter, responsible for moving Catecholamines into vesicles. Pharm-ANS-h-5 |
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NET
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aka Reuptake1
moves NE back into presynaptic terminal. the main method for terminating NE action. Blocked by many Rx's including Antidepressents and Cocaine. Pharm-ANS-h-6 |
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Reuptake1
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aka NET
moves NE back into presynaptic terminal. the main method for terminating NE action. Blocked by many Rx's including Antidepressents and Cocaine. Pharm-ANS-h-6 |
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Mechanism of Amphetamine Action
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Same mechanism as ephedrine and tyramine.
Taken into presynaptic terminal by NET, into vesicles by VMAT. Displaces NE or DA (from sequestering proteins I would guess) NE and DA concentration reverses function of VMAT and NET, spilling out into synapse. Indirect acting drug, acts only if adrenurgic innervation is intact. Repeated administration leads to tachyphylaxis. Pharm-ANS-h-6 |
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Mechanism of Ephedrine Action
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Same mechanism as amphetamine and tyramine.
Taken into presynaptic terminal by NET, into vesicles by VMAT. Displaces NE or DA (from sequestering proteins I would guess) NE and DA concentration reverses function of VMAT and NET, spilling out into synapse. Indirect acting drug, acts only if adrenurgic innervation is intact. Repeated administration leads to tachyphylaxis. Pharm-ANS-h-6 |
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Mechanism of Tyramine Action
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Same mechanism as ephedrine and amphetamines.
Taken into presynaptic terminal by NET, into vesicles by VMAT. Displaces NE or DA (from sequestering proteins I would guess) NE and DA concentration reverses function of VMAT and NET, spilling out into synapse. Indirect acting drug, acts only if adrenurgic innervation is intact. Repeated administration leads to tachyphylaxis. Pharm-ANS-h-6 |
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MAO
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monoamine oxidase metabolizes catecholomines.
located on the outer surface of mitochondria on the nerve terminal and breaks down free NE in the mobile pool. also present in liver & GI to break down circulating catecholamines and also any tyramine ingested with food Pharm-ANS-h-6 |
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COMT
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catechol-O-methyl transferase
found throughout body, esp in Liver breaks down circulating Catecholamines Pharm-ANS-h-6 |
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VMA
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3-methoxy- 4-hydroxy-mandelic acid
measured form a 24 hour urine sample used to estimate metabolism of NE & E Pharm-ANS-h-6 |
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HVA
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homovanillic acid
product of Dopamine degradation. Pharm-ANS-h-6 |
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M1 receptors
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Gq -- IP3/DAG
Increases intraceullar Ca2+ depolarizes cell Found in CNS, Exocrine Glands, GI increases secreitions Pharm-ANS-h-7 |
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M2 receptors
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Gi -- reduce cAMP
opens K+ channels hyperpolarizes cells (generally inhibitory) heart--slows some smooth muscle presynaptically--decreases NT release Pharm-ANS-h-7 |
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M3 receptors
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Gq -- IP3/DAG
Increases intraceullar Ca2+ depolarizes cell some exocrine glands (incl. salivary) -- increase secretions smooth muslce endothelium Pharm-ANS-h-7 |
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NN receptors
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Nicotininc receptors
autonomic ganglia adrenal medulla 80 A 5 subunit Na+ channel Rapidly desensitized Pharm-ANS-h-7 |
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NM receptors
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Nicotinic Receptor found in skeletal muscle
80 A 5 subunit Na+ channel Rapidly desensitized Pharm-ANS-h-7 |
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Alpha1 receptors
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Selective Agent: Phenylephrine
Gq -- IP3/DAG Increases intraceullar Ca2+ depolarizes cell Major Effects: ---vasoconstriction, increase in TPR esp in skin ---vasoconstriction = decreasing nasal congestion ---mydriasis without affecting accomodation ---prostate gland contraxn ---contract UG smm--sphincters & trigone Minor Effects ---relax intestinal smooth muscle (small effect) ---pilomotor smm: erection of hair ---increase glycogenolysis and gluconeogenesis in the liver in some species (small effect) Pharm-ANS-h-7 |
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Alpha2 receptors
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Selective agent: Clonidine
Gi -- reduce cAMP opens K+ channels hyperpolarizes cells (generally inhibitory) presynaptic terminals: inhibit NT release platelets: aggregation lipocytes: inhibit lipolysis smooth muscle: some vascular contraxn [minor inhibition of insulin and renin secretion, easily overriden by Beta] Pharm-ANS-h-7 |
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Beta1 receptors
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Isoproterenol > Epinephrine = NE
Selective Agonist: Dobutamine Gs -- increases cAMP closes K+ channels depolarizes the cell excitatory Positive Inotropic and Chronotropic Effect (Contractility & HR) Increase AV conduction velocity and automaticity Increase renin secretion Pharm-ANS-h-7 |
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Beta2 receptors
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Isoproterenol > Epinephrine >> NE
Selective Agonist: Albuterol Gs -- increases cAMP closes K+ channels depolarizes the cell tissue dependent response (excitatory/inhibitory) BP: decrease in blood pressure and a reflex increase in heart rate • cardiac effects similar to β1, but less pronounced • relaxn of respiratory, uterine, gastrointestinal smooth muscle • relaxn of blood vessels supplying skeletal muscle • relaxn of uterus • K+ uptake into skm • activate glycogenolysis and Gng in the liver • increase aqueous humor secretion • small stimulation of Insulin secretion Pharm-ANS-h-7 |
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Beta3 receptors
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Isoprotenerol = NE > Epinephrine
Gs -- increases cAMP closes K+ channels depolarizes the cell Receptors only on lipocytes Increases lipolysis Pharm-ANS-h-7 |
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D1 receptor
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with D5
Gs -- increase cAMP closes K+ channels hyperpolarizing Brain Renal Vascular Bed: Dilation Pharm-ANS-h-7 |
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D5 receptor
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with D5
Gs -- increase cAMP closes K+ channels hyperpolarizing Brain Renal Vascular Bed Pharm-ANS-h-7 |
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D2 receptor
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D2, D3 & D4
Gi -- decreases cAMP opens K+ channels depolarizing Brain Various other tissues Generally Inhibits NT release Pharm-ANS-h-7 |
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D3 receptor
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D2, D3 & D4
Gi -- decreases cAMP opens K+ channels depolarizing Brain Various other tissues Pharm-ANS-h-7 |
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D4 receptor
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D2, D3 & D4
Gi -- decreases cAMP opens K+ channels depolarizing Brain Various other tissues Pharm-ANS-h-7 |
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Alpha2A receptors
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with Alpha2C receptors
Presynaptic receptors on Noradrenergic terminals which inhibit NE release Pharm-ANS-h-10 |
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Alpha2C receptors
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with Alpha2A receptors
Presynaptic receptors on Noradrenergic terminals which inhibit NE release Pharm-ANS-h-10 |
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Presynaptic Beta receptors
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Increase NE release
Pharm-ANS-h-10 |
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Presynaptic M2 receptor on Noradrenergic Terminals
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decreases NE release
Pharm-ANS-h-10 |
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Tropotrophic
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PSNS activity: rest and digest.
All PSNS activities discretely innervated (Compare to coordinated SNS activation) Necessary for Life Pharm-ANS-ppt-32 |
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Ergotrophic
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SNS activity: fight orflight
Coordinated activation (Compare to discrete innervation of PSNS) Pharm-ANS-ppt-32 |
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ANS in the Cardiovascular System
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M2 receptors located mainly in atrium: decrease heart rate and conduction
also decreases NE release Beta1 (&Beta2) increase heart rate, AV conduction, contractility Pharm-ANS-h-12 |
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ANS receptors in the Pulmonary System
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M2 & M3 receptors cause bronchoconstriction
Beta2 relaxes bronchioles Pharm-ANS-h-12 |
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ANS receptors in the Vascular System
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Non-innervated muscarinic receptors on endothelium cause NO prodxn
Alpha1 constricts veins, blood vessels to skin and some skm blood vessels. Targetted by decongestants for constricting blood vessels in nose Beta1 increases renin secretion Beta2 relaxes blood vessels in skm and coronary arteries Pharm-ANS-h-12 |
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ANS Receptors in the eyes
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PSNS:
M3 profuse secretion from lacrimal glands M3 contraxn of ciliary muslce, decreases intraocular pressure and accomodates for near vision M3 causes miosis SNS: Alpha1: constrict radial muscles causing dilation of pupils Alpha2: reduces intraocular pressure Pharm-ANS-h-13 |
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ANS Receptors in Salivation
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PSNS: M3 Profuse salivation
SNS: Alpha one: low level salivation Pharm-ANS-h-13 |
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ANS Receptors in the GI Tract
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PSNS:
M3 stimulate contraxn of GI wall. relaxes sphincters,increases secretions SNS: Alpha2 and Beta2 relax GI tract, decrease secreitons Alpha1 contracts sphincters Pharm-ANS-h-13 |
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ANS Receptors in the UG System
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PSNS:
M3: contracts the detruser muscle, relaxes urinary sphincters and trigone M3 promotes erectrion SNS: Beta2 relax bladder and uterus Alpha1 contracts sphincters, increases motility and tone of ureter Alpha1 promotes ejaculation Pharm-ANS-h-13 |
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ANS Metabolic Effects
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Beta2 and Alpha 1 increase glycogenolysis and Gng in the Liver
Alpha 2 decrease insulin secretion Beta 3 increase lipolysis Beta 2 increase K uptake into skm Pharm-ANS-h-14 |
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Reflex Brady/Tachycardia
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Heart Rate slows down/speeds up to compensate for increases or decreases in TPR, as measured by baroreceptors.
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Photophoba
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Bright Light + Blocked Constriction Reflex
Pharm-ANS-h-15 |
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cycloplegia
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loss of accommodation
occurs if ciliary muscle is blocked with cholinurgic antagonists. Pharm-ANS-h-15 |
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What ANS drugs reduce intraocular pressure
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M3- constricts ciliar muscle-widens space in trabecular meshworkd
Alpha2- contracts radial muslce. dilates pupil promotes drainage. Beta receptors increase aqueous humor prodxn Beta blockers lower pressure Pharm-ANS-h-15 |
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Alpha1 receptor subtypes
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Alpha1A prominent in prostate
Alpha1B important in vasculature Pharm-22-pdf-7 |