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17 Cards in this Set
- Front
- Back
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Components of the Sympathetic NS:
Neurotransmitter of preganglionics-- What kind of receptors-- Result of stimulation of postganglionics-- Effects of neurotransmitter-- |
Preganglionic neurons (with ACh), ganglia, nicotinic receptor, postganglionic neuron--> NE synthesis (or Epi in adrenal medulla).
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Adrenergic Transmission:
Synthesis-- Storage-- Exocytosis-- |
*Synthesis in postganglionic neuron.
-Norepinephrine is synthesized from its precursor, dopamine. -Free norepinephrine is metabolized by monoamine oxidase (MAO) *Storage in vesicles -RESERPINE (old school BP med) blocks the uptake of NE into vesicles *Release through exocytosis -GUANETHIDINE and BRETYLIUM (also old school) block the release of NE into the synaptic cleft |
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The Mechanism by Which Cocaine Alters Sympathetic Tone:
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Blocks reuptake of NE.
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Normal NE transport:
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*80% of NE goes through NE transporter and is collected in synaptic vesicle.
*20% diffuses away and is degraded by MAO and COMT. |
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Mechanisms of Sympathetic Signal Transduction:
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*All autonomic receptors are coupled to GTP-binding proteins with second messenger system (relatively slow).
-Alpha-1 (subtypes 1A, 1B, 1D): Activate phospholipase C; Increase IP3 and Intracellular Ca++ -Alpha-2 (subtypes 2A, 2B, 2C): Inhibition adenylyl cyclase and decrease cAMP -Beta-1/Beta-2: Stimulate adenylyl cyclase and increase cAMP *Different receptors--> different effects. |
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Relative Receptor Potencies of Norepinephrine and Epinephrine:
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Alpha-1: EPI ≥ NE
Alpha-2: EPI ≥ NE Beta-1: EPI = NE Beta-2: EPI >> NE Beta-3: NE > EPI *ß2 receptors are the big difference! Epi is much more potent; enables NE to be used as a therapy...more to come. |
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Effects of Stimulation of Beta-1 Adrenoreceptors:
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*Heart * (think heart!)
-SA Node: Increased heart rate -AV Node: Increased conduction velocity -HIS-purkinje cells: Increased conduction velocity and automaticity -Cardiac Muscle: Increased contractility *Kidney juxtaglomerular cells-- Increased renin secretion *Some beta-2 and beta-3 effects in the heart. Biggest effect is from ß1. |
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Effects of Stimulation of Beta-2 Adrenoreceptors :
Effects of Stimulation of Beta-3 Adrenoreceptors : |
*Smooth Muscle (think relaxation!)
Arteriolar: Relaxation Bronchiolar: Relaxation Intestinal: Relaxation (reduced motility) Genitourinary: Relaxation (reduced urgency) *Other Muscle: Ciliary muscle (eye): relaxation Skeletal muscle: increased potassium uptake *Liver: Increased glycogenolysis *Pancreatic Islets (Beta Cells): Increased insulin secretion *Stimulation of Beta-3 Adrenoreceptors: Lipolysis and Smooth Muscle Relaxation |
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Effects of Stimulation of Alpha-1 Adrenoreceptors :
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Smooth Muscle
Arteriolar*: Contraction Veins*: Contraction Genitourinary: Contraction Intestinal: Relaxation Eye Radial muscle: Contraction Lacrimal glands: Secretion Liver-- Increased glycogenolysis Kidney juxtaglomerular cells-- Decreased renin secretion *Some alpha-2 effects as well here, but mostly alpha-1 |
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Effects of Stimulation of Alpha-2 Adrenoreceptors :
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*Pancreatic Islets (Beta Cells)
Decreased insulin secretion *Presynaptic Receptors Decreased release of norepinephrine |
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Components of the Parasympathetic NS:
Neurotransmitter of preganglionics-- What kind of receptors-- Result of stimulation of postganglionics-- Effects of neurotransmitter-- |
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Cholinergic transmission:
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Synthesis:
*Choline uptake (which is reduced by hemicholinium); combines with acetyl CoA in presence of choline acetyltransferase (CHAT) produces acetylcholine *Storage in vesicles (Uptake reduced by vesamicol) *Release through exocytosis (Blocked by botulinum toxin) *Binding to receptors (postsynaptic) *Removal from synaptic cleft: Acetylcholinesterase (AChE) is primary means of removal of ACh in synaptic cleft. Choline + Acetate are taken back up into presynaptic neuron. Reuptake of ACh is relatively SMALL. |
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Muscarinic Receptors (M1-M5) and Mechanisms of Signal Transduction I:
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*G-protein coupled receptors: 2nd messenger system with slower response than nicotinic receptors
-M1, M3, M5: all increase release of intracellular calcium and protein phosphorylation; M2, M4: both increase potassium permeabilty and decrease cAMP *M2 -Location: Heart: SA node, Atria, AV node, Ventricles -Result of Stimulation: Increased potassium permeability (inhibitory); Decreased adenylyl cyclase activity (decreased cAMP); Decreased calcium permeability: Slows conduction *There are no specific (M1, M2...) drugs for these! Just anti-muscarinics. |
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Muscarinic Receptors (M1-M5) and Mechanisms of Signal Transduction II:
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M3
Location/Result of Stimulation: Smooth muscle contraction; Relaxation of sphincters; Dilation of vessels through production of NO by vascular endothelium; Increased secretion of glands M1, M4, M5 *There are no specific (M1, M2...) drugs for these! Just anti-muscarinics. |
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Stimulation of Muscarinic Receptors I:
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*Heart
SA Node: Decreased heart rate AV Node: Decreased conduction velocity Muscle: Decreased contractility (vagus is responsible for all of these effects) *Vascular Smooth Muscle Endothelium intact: Relaxation Endothelium removed: Contraction |
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Stimulation of Muscarinic Receptors II:
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*Other Smooth Muscle
Gastrointestinal: Contraction Bronchiolar: Contraction *Eye Sphincter muscle: Contraction Ciliary muscle: Contraction *Glands: Increased secretion Salivary; Lacrimal; Nasopharyngeal; Bronchiolar; GI; Pancreatic digestive glands; Skin sweat glands *Sphincters Urinary: Relaxation Gastrointestinal: Relaxation |
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Discuss the Baroreceptor Reflex Arc:
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Stand up --> bp falls --> leads to vasoconstriction (alpha), cardiac stimulation (ß1), and inhibition of cardiac inhibitor.
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