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79 Cards in this Set
- Front
- Back
What are always the first neurotransmittes and receptors?
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Ach on nicotinic receptors.
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Adrenal gland innervation and secretion
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Adrenal gland is innervated by sympathetic innervation via Ach on nicotinic receptors. Gland then secretes 80% epi and 20% nori
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What connects the ENS and CNS
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ANS
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Myenteric plexus
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AKA Aurbachs. ENS nerve plexus. Found between smooth muscle layers in the gut. Influence motility.
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Submucosal Plexus
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AKA Miesners. ENS nerve plexus. Stimulate epithelial secretion.
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ICC
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Intersticial cell of cajal. Mediates neurotransmission of ENS and acts as the pacemaker.
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NTS
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Nucleus tractus solitarius. Major visceral relay center in the brain. Is where all autonomic sensory info comes in. This info is then sent to the CNS autonomic network to cause effects.
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Area Postrema
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Located outside BBB, senses glucose, plasma electrolites, hormones, and CNS chemicals. Gives its info to the NTS.
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What is considered the principle integrative center for the ANS?
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Hypothalamus
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What is the neurotransmitter of all autonomic ganglia?
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Ach
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ATP as a co transmitter
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Cotrnasmitter for both sympathetic and para neurons. Is the fast transmitter.
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NPY
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Neuropeptide Y, Cotransmitter in sympathetic neurons. Is slow response.
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VIP
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Vasoactive intestinal peptided. Co transmitter in parasympathetic nerves. Is slow response.
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Nicotinic 1 vs 2 Location
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2 is for the NMJ, everything else is 1.
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Eye Sympa response
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Iris Radialis muscle: A1 - Contraction (mydriasis)
Ciliary Muscle: B2 - Relaxation, stretching lens for far vision. |
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Eye Para response
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Iris Sphyncter muscle: M3 - Contraction (miosis)
Ciliary muscle: M3 - Contraction for near vision (accommodation) Lacrimal Glands: M3 - Secretion. |
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Heart Sympa response
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All B1:
SA node - Increases HR (chronotropic) Atria - Increase Contractility (Inotropic) AV Node - Increases Automaticity HIS purkinje - Increases Automaticity. Ventricle - Increases Contractility, automaticity and idioventricular pacemaker rate. All other than SA node also increase conduction velocity. |
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Heart para response
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All are M2:
SA node - Decrease HR Atria - Decrease contractility and shorten AP duration AV node - Decrease conduction velocity and AV block. HIS purkinje - Little effect Ventricle - Slight decrease in contractility. |
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Blood vessel Sympa response
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Skeletal Muscle: B2 - Dilation
Coronary: A1 - Constriction Viscera: " Skin: " Brain: " Erectile Tissue: " Salivary Glands: " Veins: " |
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Blood vessel para response
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Erectile tissue: M3 - Dilation
Salivary Glands: M3 - Dilation |
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Effects of cGMP/AMP
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Increase always leads to relaxation except in heart where it causes contraction.
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Lung Sympa stimulation
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Bronchial SM: B2 - Relaxation
Bronchial Glands: A1 - Decrease secretion Bronchial Glands: B2 - Increase secretion |
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Lung para stimulation
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Bronchial SM: M 2=3 - Contraction
Bronchial Glands: M3, M2 - Increased secretion. |
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GI sympa stimulation
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Motility: A1,2 and B1,2 - Decrease
Sphincters: A1 - Contraction Secretion: A2 - Inhibition |
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GI Para stimulation
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Motility: M2 = M3 - Increase
Sphincters: M3, M2 - Relaxation Secretion: M3, M2 - Stimulation |
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Gall bladder sympa and para stimulation
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Sympa: B2 - Relaxation
Para: M - Contraction |
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Uterus Sympa and para stimulation
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Sympa:
Contraction - A1 Relaxation - B2 Para: Maybe relaxation - M |
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Kidney sympa and para stimulation
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Sympa: JG cells: B1 - Increase renin secretion
Para: No innervation |
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Male sex organ sympa and para stim
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Sympa: A1 - Ejaculation
Para: M3 - Erection |
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Skin and sweat sympa and para stim
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Sympa:
Pilomotor muscles: A1 - Contraction Loccalized sweat glands (apacrine): A1 - Secretion Sweat glands: Generalized secretion - M3, M2 |
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Spleen sympa and para stim
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Sympa:
A1 - Contraction B2 - Relaxation Para = none |
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Liver symp and para stim
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Sympa:
Glycogenolysis - A1 Gluconeogenesis - B2 Para = none |
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Pancrease para and sympa stim
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Sympa:
Acini: A - Decrease secretion Islet (beta) cells: A2 - Decreased secretion B2 - Increased secretion Para: Acini cells: M3, M2 - Increase Secretion. |
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Salivary gland sympa and para stimulation
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Sympa: A1 - K+ and water secretion
Para: M3, M2 - K+ and water secretion |
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Bladder sympa and para stim
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Sympa:
Detrusor: B2 - Relaxation Trigone: A1 - Contraction Para: Detrusor: M3 - Contraction Trigone: M3 - Relaxation |
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What are the autoreceptor negative feedback receptors?
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A2 for nori, M2 for Ach
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Ach life cycle
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1) Choline trnasported into cell
2) AcCoA + Choline > Ach (via ChAT) 3) Molecules of Ach are packaged inside vesicles 4) Calcium causes release of vesicles 5) Ach binds to receptors and autoreceptors 6) Ach is inactivated by Ach esterase in synapse forming cholinie and acetate. Choline can be reused. |
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Describe the sympathetic innervation to the sweat glands
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Post ganglionic neurons involved with stress sweat secretion secrete nori (sweaty palms)
Post ganglionic neurons involved with thermoregulation release Ach |
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Describe the sympa innervation to the SM of the renal vascular bed
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Post gaglionic neurons to the SM of the renal vascular bed secrete dopamine.
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Heteroreceptors
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Are feedback receptors (like autoreceptors) which are activated by other nearby neurons.
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What is the most important inactivation process for cholinergic neurons?
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Breakdown via Ach esterase
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Do blood vessels have cholinergic receptors?
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Yes, they have muscarinic receptors despite the lack of para innervation. Important when giving drugs.
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M1 G protein activation process (M3,5 as well)
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1) Gq
2) Activation of PLC 3) Increase in IP3 leads to increase of calcium; Increase in DAG leads to an increase of PkC 4) Increase in calcium causes contraction |
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M2 G protein activation process (M4 as well)
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1) Gi
2) Inhibition of adenyl cyclase 3) Decrease in cAMP 4) Activation of K+ channels 5) Inhibition of voltage gated Calcium channels 6) Hyperpolarization and inhibition. |
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Vesamicol (mechanism and effect)
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Inhibition of vesicular uptake of Ach. Decrease effect.
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Botulinus toxin (mechanism and effect)
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Inhibits fusion and release. Decreases effect.
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Hemicholinium (mechanism and effect)
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Blocks choline transport system. Decreases effect.
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Bromopyruvate (mechanism and effect)
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Inhibits pyruvate dehydrogenase (in mitochondria) leading to a reduction in Actyl CoA. Decreases effect.
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Nicotine (mechanism and effect)
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Nicotinic agonist. Increases effect.
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Trimethaphan (mechanism and effect)
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Nicotinic antagonist. Decreases effect.
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Pilocarpine (mechanism and effect)
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Muscarinic agonist. Increases effect.
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Atropine (mechanism and effect)
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Muscarinic antagonist. Decreases effect.
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Neostigmine (mechanism and effect)
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Ach esterase inhibitor. Increases effect.
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Norepinephrine Life cycle
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1) Tyrosine transported into the cell
2) Tyrosine converted to Dopa via tyrosine hydroxylase (RLS) 3) Dopa converted to dopamine via dopa decarboxylase 4) Dopamine is transported into vesicles via VAC 5) While being transported, dopamine is converted to nori via dopamine B hydroxylase 6) Calcium causes release of nori 7) Nori binds to postsynaptic receptors, alpha autoreceptors (-) and beta autoreceptors (+) 8) Nori is cleared via reuptake into nerve terminal (uptake 1) and into postsynaptic neuron (uptake 2). |
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Tyrosine hydroxylase (function, specificity, location)
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1) Converts tyrosine to dopa (RLS)
2) Specific for L tyrosine 3) Widespread, present in sympathetic nerves |
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Aromatic-l-amino acid decarboxylase
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1) Converts dopa to dopamine. Inhibition doesnt really have an effect.
2) Non-specific 3) Widespread, found in sympathetic nerves. |
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Dopamine B hydroxylase
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1) Converts dopamine to nori. Inhibition can decrease lvls of nori and epi.
2) non-specific 3) Widespread, present in sympa neurons |
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Phenyl-enthanolamine n-methyl transferase
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Converts Nori to Epi. Under control of glucocorticoid
Largely in adrenal gland. |
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Heteroreceptor and autoreceptor overview
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1) Both Nori and Ach block their own release via autoreceptors
2) Ach blocks Nori release via heteroreceptor 3) Nori blocks Ach and NPY release via heteroreceptor and autoreceptor 4) NPY blocks Ach and Nori release via heteroreceptors and autoreceptors. |
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MAO (Function, location, subcellular location)
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1) Reduces nori levels
2) Found both neuronal and extra neuronal. Neuronal in adrenal medulla. Extra in liver and brain. 3) Found in mitochondria |
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COMT (Function, location, subcellular location)
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1) Breaks down nori, extraneuronaly only. Regulates extraneuronal and circulating calcium levels. Inhibition does nothing.
2) Widespread in liver and kidney, extraneuronal. 3) Cytosolic. |
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A1 A2 B1 B2 generalizations
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A1 - Excitatory
A2 - Inhibatory B1 - Excitatory B2 - Inhibatory |
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A1 effector pathway
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1) Gq
2) Activation of PLC 3) Increased IP3 and DAG 4) Increased calcium 5) Increased contractility |
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A2 effector pathway
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1) Gi
2) Inhibition of adenyl cyclase 3) Decrease in cAMP 4) Inhibition of PkA |
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Epinephrin (agonist/antag and selectivity)
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Agonist. No selectivity
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Norepinephrine (agonist/antag and selectivity)
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Agonist, Alpha 1,2 and B1 selectivity.
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Isoproterenol (agonist/antag and selectivity)
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Agonist, B1, B2 selectivity
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Dopamine (agonist/antag and selectivity)
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Agonist, dopamine selectivity.
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Phenylephrine (agonist/antag and selectivity)
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Agonist, A1 selectivity.
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Clonidine (agonist/antag and selectivity)
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Agonist, A2 selectivity
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Dobutamine (agonist/antag and selectivity)
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Agonist, B1 selectivity
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Terbutaline (agonist/antag and selectivity)
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Agonist, B2 selectivity
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Phentolamine/Phenoxybenzamine (agonist/antag and selectivity)
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Antagonist, A1, A2 selectivity
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Prazosin (agonist/antag and selectivity)
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Antagonist, A1 selectivity.
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Yohimbine (agonist/antag and selectivity)
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Antagonist, A2 selectivity
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Propranolol (agonist/antag and selectivity)
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Antagonist, B1, B2 selectivity
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Metoprolol (agonist/antag and selectivity)
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Antagonist. B1 Selectivity
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Butoxamine (agonist/antag and selectivity)
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Antagonist, B2 selectivity.
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Generalizations on what aspects of the autonomics the brain stem, limbic system, and cortex are involved in.
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Bran stem - Refelx control of vital functions
Limbic system - Intergration of emotional state with visceral activities Cortex - Integrates somatic and visceral functions. |