Introduction To Autonomic Pharmacology

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anatomical characteristics of parasympathetic nerve fibers

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-originates craniosacral
nerve fibers are long preganglionic; short postganglionic
-Ganglia is located in tissue innervated

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anatomical characteristics of sympathetic nerve fibers

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-originates thoracolumbar
nerve fibers are short preganglionic; long preganglionic
-ganglia is located in two paravertebral chains on either side of spinal column

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anatomical characteristics of somatic nerve fibers

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only one neuron

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ALL autonomic preganglionic neurons are _______.

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cholinergic

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ALL parasympathetic postganglionic neurons are _______.

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cholinergic

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MOST sympathetic postganglionic neurons are _________.

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adrenergic

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The adrenal medulla is a modified _______.

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sypathetic ganglion

Front 8

“Effector” cells are (give 3)

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cardiac mm, smoothe mm, gland cells, and sometimes endothelial cells and nerve terminals

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Describe biosynthesis of Ach

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synthesized in cytoplasm from acetyl-CoA and choline through catalytic action of enzyme choline acetyltransferase (ChaT)

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storage of Ach

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Ach transported from cytoplasm into vesicles by antitransporter that removes protons. A "quanta" of Ach in each vesicle"

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release of Ach

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dependent on extra cellular Ca2+. When AP reaches terminal and triggers sufficient influx of Ca2+. Vesicles fuse with membrane and spit out Ach.

Front 12

metabolism of acetylcholine in the cholinergic junction.

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Acetyl cholinesterase (AChE) splits Ach into choline and acetate.

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biosynthesis of NE

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Tyrosine transported into the noradernegic ending by sodium dependent carrier. Tyrosine converted to dopamine which is transported into the vesicle by a carrier. Dopamine is converted to NE in the vesicle by dopamine B hydroxylase.

Front 14

release of NE

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action potential opens voltage-sensitive Ca2+ channels and increases intracellular Ca. Vesicles fuse w/ surfuse membrane and results in expulsion of NE.

Front 15

metabolism of NE

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NE diffuses out of cell or is transported into cytoplasm of terminal or postjunctional cell.

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parasympathetic presynaptic NT & receptor

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Ach;cholinoreceptor (Ach receptor)

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parasympathetic postsynaptic NT & receptor

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Ach;cholinoreceptor (Ach receptor)

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sypathetic presynaptic NT & receptor

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Ach;cholinoreceptor (Ach receptor)

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Sympathetic postsympathetic NT & receptor

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NE; Adrenoreceptors

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motor end plate NT & receptor

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Ach;cholinoreceptor (Ach receptor)

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role and location of (cholinocereptors) Muscarinic M1

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CNS

results in formation of IP3 & DAG, increased intracellular Ca

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role and location of (cholinocereptors) Muscarinic M2

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MYOCARDIUM

FUNCTIONS IN OPENING OF POTASSIUM CHANNELS, INHIBITION OF ADENYL CYCLASE

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role and location of (cholinocereptors) Muscarinic M3

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smooth muscles and glands

Formation of IP3 & DAG, increased intracellular calcium

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role and location of (Adrenoceptors) alpha1 A1

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postsynaptic effector cells, especially smooth mm

Formation of IP3 & DAG, increased intracellular CA

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role and location of (Adrenoceptors) alpha2 A2

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Presynaptic adrenergic nerve terminals (autoreceptors)

Inhibition of adenylyl cyclase, decreased cAMP

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role and location of (Adrenoceptors) Beta1 B1

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heart

Stimulation of adenylyl cyclase, increased cAMP

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role and location of (Adrenoceptors) Beta2 B2

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smooth mm

Stimulation of adenylyl cyclase, increased cAMP

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role and location of (Adrenoceptors) Beta3 B3

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fat cells

Stimulation of adenylyl cyclase, increased cAMP

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Nicotinic NN
Typical location & result of ligand binding

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Postganglionic neurons, some presynaptic cholinergic terminals

Opening of Na+, K+ channels, depolarization

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Nicotinic NM

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Skeletal muscles neuromuscular end plates

Opening of Na+, K+ channels, depolarization

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D1 (DA1) & D5

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Brain & smooth muscles of renal vascular bed

Stimulation of adenylyl cyclase, increased cAMP

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D2 (DA2)

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Brain & smooth muscles of renal vascular bed

Inhibition of adenylyl cyclase, decrease cAMP

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Local anesthetics, tetrotoxin, saxitoxin

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blocks ACTION POTENTIAL PROPAGATION by acting on nerve axons to block sodium channels and thus block conduction.

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hemicholinium

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prevents TRANSMITTER SYNTHESIS by acting on CHOLINERGIC nerve terminals at the membrane to block the uptake of choline

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alpha-methyltyrosine (metyrosine)

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prevents TRANSMITTER SYNTHESIS by acting on ADRENERGIC nerve terminals and the adrenal medula at the cytoplasm to block NT synthesis

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Vesamicol

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prevents TRANSMITTER STORAGE by by acting of the vesicles in CHOLINERGIC TERMINALS

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Reserphine

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prevents TRANSMITTER STORAGE by by acting of the vesicles in ADERNERGIC TERMINALS

Front 38

Norepinephrine, dopamine, acetylcholine, angiotensin II, various prostaglandins

Back 38

Effects TRANSMITTER RELEASE by acting on nerve terminal membrane receptors to modulate release

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omega-Contoxin GVIA

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Reduces TRANSMITTER RELEASE by acting on nerve terminal calcium channels to reduce transmitter release

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BOTULINUM TOXIN

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Prevents TRANSMITTER RELEASE by acting on CHOLINERGIC vesicles to prevent release

Front 41

Alpha latrotoxin

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Effects TRANSMITTER RELEASE by acting on CHOLINERGIC and ADENERGIC vesicles causing an explosive release of NT

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Tyramine, amphetamine

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Promotes TRANSMITTER RELEASE by acting on ADRENERGIC nerve terminals to promote transmitter release

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Cocaine, Tricyclic antidepressants

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Inhibits TRANSMITTER UPTAKE AFTER RELEASE by acting on ADRENERGIC nerve terminals to inhibit uptake and increasing transmitter effect on postsynaptic receptors

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6 Hydroxydopamine

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Effects TRANSMITTER UPTAKE AFTER RELEASE by destroying ADRENERGIC nerve terminals

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Norepenephrine

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Causes RECEPTOR ACTIVATION by acting on receptors at ADENERGIC junctions by binding to alpha receptors causing activation

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Phentolamine

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Causes RECEPTOR BLOCADE by acting on receptors at ADENERGIC junctions by binding to alpha receptors preventing activation

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Isoproterenol

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Causes RECEPTOR ACTIVATION by acting on receptors at ADENERGIC junctions by binding to beta receptors causing activation of adenylyl cyclase

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Propranolol

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Causes RECEPTOR BLOCADE by acting on receptors at ADENERGIC junctions by binding to beta receptors preventing activation

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Nicotine

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Causes RECEPTOR ACTIVATION by binding to receptors at nicotinic CHOLINERGIC junctions (autonomic ganglia, neuromuscular end plates) to bind nicotinic receptors opening ion channels in post synaptic membrane

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Tubocurarine

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Causes RECEPTOR BLOCKADE by acting on neuromuscular end plates to prevent activation

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Bethanechol

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Cuaes RECEPTOR ACTIVATION by acting receptors of parasympathetic effector cells (smooth mm, glands) to bind and activate muscarinic receptors

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Atropine

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Causes RECEPTOR BLOCKADE by acting receptors of parasympathetic effector cells (smooth mm, glands) to bind and inactivate muscarinic receptors

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Neostigmine

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Prevents ENZYMATIC INACTIVATION OF TRANSMITTER by acting on CHOLINERGIC synapses (acetylcholinesterase) to inhibit enzyme and prolong and intensify transmitter action

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Tranylcypromine

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Prevents ENZYMATIC INACTIVATION OF TRANSMITTER by acting on ADRENERGIC nerve terminals (monoamine oxidase) to inhibit enzyme; and increase stored transmitter pool

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Stimulation of Parasympathetic innervation of the CIRCULAR (sphincter)of the iris: effect & receptor

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contraction - miosis –M3

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block of stimulation of Parasympathetic innervation of the CIRCULAR (sphincter mm)of the iris: effect & receptor

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dilation – mydriasis -M3

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Stimulation of sympathetic innervation of the RADIAL smooth mm of the iris (dialator mm): effect & receptor

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dilation – mydriasis - alpha1

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Block of stimulation of sympathetic innervation of the RADIAL smooth mm of the iris (dialator mm): effect & receptor

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contraction - miosis –alpha1

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Stimulation of Parasympathetic innervation of the ciliary body (smooth mm): effect & receptor

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contracts – relaxes suspensory ligaments- allows lens to widen – focus for near vision (M3)

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Block stimulation of Parasympathetic innervation of the ciliary body (smooth mm): effect & receptor

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cycloplegia inabilidate to accomidate for near vision (M3)

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Stimulation of sympathetic innervation of the ciliary body (smooth mm): effect & receptor

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not under sympathetic control

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Function of canal of schlemm and results of blockage

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drainage of aqueous humor of the eye. If blocked, accumulation of AH results and increase intra ocular pressure. This can cause blindness.

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Parasympathetic and sympathetic considerations at the canal of schlemm

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Stimulation of cholenergic fibers will increase drainage

If you block Ach, you decrease drainage and glaucoma results.

Beta blockers interfere w/ production of aqueous humor and are bennifiial for glaucoma.

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Stimulation of Parasympathetic innervation of the bladder : effect & receptor

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contraction of detrusor mm (bladder wall)--M3, relaxation trigone mm (sphincter)--M3; Result is peeing

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Stimulation of Parasympathetic innervation of the bladder : effect & receptor

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urinary retention -- M3

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Stimulation of sympathetic innervation of the bladder : effect & receptor

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relax detrusor mm(B2), constrict trigone mm (a1) causes urinary retention

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Block stimulation of sympathetic innervation of the bladder : effect & receptor

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not too much effect cuz parasymp predominates

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Stimulation of Parasympathetic innervation of the GI tract: effect & receptor

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increase GI motility and tone and relaxation of sphincters and increase in secretion of exocrine glands (m3)

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Blocked stimulation of Parasympathetic innervation of the GI tract: effect & receptor

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constipation (m3)

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Stimulation of sympathetic innervation of the GI tract: effect & receptor

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constriction of smooth mm walls - b2, constriction of sphicter a1 - constipation

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Stimulation of sympathetic innervation of the GI tract: effect & receptor

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minimal effect – parasymp predominates

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Stimulation of sympathetic innervation of the heart: effect & receptor

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increae conduction at SA & AV node, & contraction of ventrical results in increae heart rate -- beta1

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Block stimulation of sympathetic innervation of the heart: effect & receptor

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decrease conduction and heart rate (e.g., beta blockers)

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Stimulation of parasympathetic innervation of the heart: effect & receptor

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L vagus nn-av node-receptor decrease HR (m2) , R vagus nn –sa node- decrease HR(m2)-, no fibers to ventricle.

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Stimulation of parasympathetic innervation of the blood vessels: effect & receptor

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No fibers to blood vessels but some M receptors present

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Block stimulation of parasympathetic innervation of the heart: effect & receptor

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increase HR increase conduction --M2

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_______ innervation predominates in the heart

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parasympathetic

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Stimulation of sympathetic innervation of the skin and visceral organ blood vessels: effect & receptor

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constriction of blood vessels -- alpha1

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Stimulation of sympathetic innervation of the skeletal mm blood vessels: effect & receptor

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relaxation of blood vessels -- beta2

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List the determinants of blood pressure

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??

Front 81

and describe how the baroreceptor reflex mechanism functions when blood pressure rises or falls

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