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79 Cards in this Set

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Synthesize, store, and release NE. Postganglionic sympathetic fibers to smooth muscle, heart, and glands. Chromaffin cells in the adrenal medulla are modified ganglion cells and release primarily Epi into circulation.
Transport a precursor molecule into the nerve ending, then synthesize the catecholamine transmitter, and finally store it in membrane-bound vesicle.
Describes receptors that respond to cathecholamines
o - I.e.: Norepinephrine.
refers to NE from neurons and epinephrine from adrenal medulla. Receptors innervated by adrenergic nerves, activated by NE
o - Alpha 1, 2
o -Beta 1, 2
Alpha 1 - stimulates all contraction of smooth muscle
Beta 2 - Relaxes smooth muscle
(gut, airways, bladder) contain nerve fibers that do not show the histochemical characteristics of either cholinergic or adrenergic fibers.

o -Tissue: Cardiac Muscle
Smooth Muscle
Vascular Endothelium
Exocrine Glands
Presynaptic Nerve Terminals
o -Cells:
(negative feedback)response to mean arterial pressure causes decreased sympathetic outflow to the heart and a powerful increase in parasympathetic (vagus nerve) discharge at the cardiac pacemaker. In the diagram green lines denote inhibitory effects and red lines indicate excitatory effects.
Large number of peripheral autonomic nervous system fibers that synthesize and release AcH, receptors activated by Ach (Nicotinic and Muscarinic), and drugs that effect neurotransmitters by Ach.
Denotes receptors (both muscurinic and nicotinic) that respond to AcH. Parasympathetic response to organ or tissue fxn. Fibers synthesize, store, and release Ach.
Receptor innervated by cholinergic nerves
Renal vascular smooth muscle and CNS. A possible postganglionic sympathetic transmitter in the renal blood vessels. Probably a modulatory transmitter in some ganglia and the ENS.
The bodies autonomic response to a drugs action. I.e., Norepi. Body “reflexors” with the opposite response of the drug. Causes acceleration of heartbeat following the stimulation of local muscle spindles when blood pressure in the venae cavae and right atrium is increased. A response that tends to compensate for any change in variable contributing to mean arterial pressure. Eg- a drug-induced increase in peripheral vascular resistance.
Crainosacral, Energy conserving. Part of the nervous system that slows the Heart rate, decreases BP, increases intestinal and gland activity, empties bladder, protects retina, and relaxes sphincter muscles. Cholinergic drugs are drugs that produce same affects.
a sensor on the surface of a neuron. It captures messenger molecules from the nervous system-neurotransmitters and thereby functions in transmitting info from one neuron to another. Each receptor is neurotransmitter specific
Receptors located on presynaptic terminals at synapses. Activated by NE, activation diminishes further release of NE.
Part of ANS originating in thoracic and lumbar regions of spinal cord that in general inhibit or oppose physiological effects of parasympathetic system. Epi released from adrenal medulla during exercise, excitement, fear, anger, etc. Preganglionic - Cholinergic Ach. Postganglionic - Adrenergic NE. Reduces the digestive secretions, speeding up the HR, dilates bronchioles and pupils, and contracting blood vessels.
are poorly absorbed and poorly distributed into the CNS becasue they're hydrophilic. Although all are hydrolyzed in the GI tract (and less active by the oral route), they differ markedly in their susceptibility to hydrolysis by cholinesterase in the body. See table 7-2 for the 5 examples the book discusses.
occurs when there is too much cholinesterase inhibition. Clinical features include: muscle fasciculation, sweating, excessive salivation, and constricted pupils. Anticholinesterases are withdrawn and atropine given. Muscular weakness resulting from depolarization block due to overdosage of anticholinesterase agents used for myasthenia gravis; similar to but different from myasthenic crisis.
A large group of drugs that mimic acetylcholine; comprised of acetylchoine receptor stimulants and cholinesterase inhibitors; can bind directly to (and activate) cholinoceptors or can act indirectly by inhibiting the hydrolysis of endogenous acetylchoine; its parasympathomimetic action occurs through an action on receptors at effector cells, not those in ganglia; directly bind to and activate muscarinic or nicotinic receptors.
refers to the contraction of the ciliary muscle in the eye, in the
accommodation of focus for near vision. May also exert tensions on
the trabecular meshwork,opening the pores & facilitating outflow of the aqeous
humour into the canal of Schlemm. The increase in aqeous humour outflow is
desirable for patients with glaucoma.
(pg96) divided on the basis of chemical structure into esters of choline (including Ach) and alkaloids (muscarinic and nicotinic). Many drugs are selective for muscarinic and nicotinic receptors and have effects on both receptors, but Ach is typical.
was the tentative name of what was later discovered to be nitric oxide (NO). It is released by the vascular endothelium in response to a variety of chemical (muscurinic agonist) and physical stimuli. Activates guanylyl cyclase and increases cGMP in smooth muscle. It causes the smooth muscle in the vessel wall to relax, resulting in vasodilation.
Drugs that inhibit cholinesterase enzymes and allow acetylcholine released from cholinergic nerves to accumulate, bind to and stimulate postsynaptic cholinergic receptors. Therefore, these agents act indirectly to “amplify” the acetylcholine signal resulting from activity of cholinergic nerves.
a drug that activates a muscarinic receptor. Examples include msucarine and acetylcholine.
A severe form of Myasthenia Gravis that must be distinguished from excessive drug therapy (cholinergic crisis), usually occuring in very ill myasthenic patients and must be managed in hospital with a ventilator available
Myasthenia Gravis
a disease affecting skeletal muscle neuromuscular junctions. An autoimmune process causes production of antibodies that decrease the number of functional nicotinic receptors on the postjunctional end plates. Findings include: ptosis, diplopia, difficulty speaking and swallowing, and extremity weakness. Found on page 104-105 under Neuromuscular Junction
a ganglionic stimulant and a ganglionic blocker. Initial effects are to stimulate ganglia. Prolonged stimulation or high doses desensitizes the nicotinic receptor, producing ganglionic blockade.
are among a group of commonly used cholinesterase inhibitors. They are organic derivatives of phosphoric acid. Many are highly lipid-soluble liquids. All except echothiophate are distributed to all parts of the body, including the CNS. These agents are often used as insecticides and poisoning with them will cause nervous system toxicity.
one of the oxygen-phosphorus bonds of the inhibitor is broken, further strengthening the phosphorus-enzyme bond. Pg.103.
havig an effect similar to that resulting from stimulation of the parasympathetic nervous system, an example of a substance that demonstrates this is the alkaloid muscarine.
the action of certain medications that inhibit the transmission of parasympathetic nerve impusles and thereby reduce spasms of smooth muscle (such as that, for example, in the bladder)
a kind of toxicity having a muscarinic effect of inhibition of sweating
a reaction that causes the face to become "beet red", not harmful
It’s a second class of compounds, capable of regenerating active enzyme from the organophosphorous-cholinesterase complex, is also available to treat organophosphorus poisoning.
a very important ocular effect of antimucarinic drugs. It is defined as the weakening of the contraction of the ciliary muscle of the eye. The result is the LOSS OF THE ABILITY TO ACCOMMODATE (usually due to the application of atropine to the eye to dilate the pupil to view the back of the eye--mydriasis.) Is useful in ophthalmology, but is also potentially hazardous, since acute glaucoma may be precipitated in patients with a narrow anterior chamber angle.
neuromuscular blocking drugs that interfere with transmission at the neuromuscular end plate and lack central nervous system activity. The clinically useful prototypical drug is succinylcholine which reacts with the nicotinic receptor to open the channel and causes depolarization of the motor end plate and this in turn spreads to the adjacent membranes, causing contractions of muscle motor units.
an agent which induces constriction of the pupil
an agent which induces dilation of the pupil
competitive agents that compete with acetylcholine for nicotinic receptors at the neuromuscular junction. These agents decrease the end-plate potential so that the depolarization threshold is not reached. Can cause respiratory paralysis. Example: Tubocurarine, Gallamine & Percuronium
Relating to substance that annuls or antagonises the affects of the parasympathetic nervous system; e.g., atropine.
describes the category of drug whose original or most common use and intended therapeutic effect is to prevent weight gain or to promote weight loss by reducing appetite for food
important endogenous regulator of hormone secretions from a number of glands in the symathetic nervous system; ex: epinephrine, norepinephrine, dopamine, and adrenaline
Medication that shrinks swollen nasal tissues to relieve symptoms of nasal swelling, congestion and mucus secretion.
an amphetamine that stimulates the CNS. Its Pharmacokinetics are similar to ephedrine but readily enters the CNS. It causes effects on mood, alertness and decreased appetite. Its peripheral actions are mediated primarily through the release of catecholamines.
means that a drug may preferentially bind to one subgroup of receptors at concentrations too low to interact extensively with another subgroup. See Table 9-2 Alpha agonists include the following: Phenylephrine and methozamine (alpha 1) Clonidine and methylnorepinephrine (alpha 2) p124
means that a drug may preferentially bind to one subgroup of receptors at concentrations too low to interact extensively with another subgroup. See Table 9-2. Beta agonist include Dobutamine, Isoproterenol, Terbutaline, metaproterenol, albuterol, and ritodrine. Pg 124.
class of drugs whose properties mimic those of a stimulated sympathetic nervous system. They increase cardiac output, dilate bronchioles, and usually cause constriction of blood vessels. Include epinephrine, norepinephrine, and other catecholamines.
to prevent the absorption of a previously secreted substance
a substance that competitively binds to a receptor site and thus prevents the attachment of another drug.
illustrates how the activation of both alpha and beta receptors in the same tissue may lead to opposite responses. For instance in the case of an agonists with both alpha and beta effects, such as epinephrine, selective alpha 1 receptor antagonism can convert a presser response to a depressor response.
The property of a drug that causes activation of adrenergic receptors so as to produce effects similar to stimulation of the sympathetic nervous system.
is a prominent effect of several beta-blockers. This action is the result of typical local anesthetic blockade of sodium channels and can be demonstrated experimentally in isolated neurons, heart muscle, and skeletal muscle membrane. However, it is unlikely that this effect is important after systemic administration of these drugs, since the concentration in plasma usually achieved by these routes is too low for the anesthetic effects to be evident.
sudden low blood pressure that occurs when a person assumes a standing position. It may be caused by hypovolemia (a decreased amount of blood in the body) resulting from the excessive use of diuretics, vasodilators, or other types of drugs, or prolonged bed rest.
are sometimes used as antagonists because they competively inhibit the responses produced by full agonists. They produce a negative response at full receptor occupancy than do full agonists. In effect, they act as weak agonists which in turn also gives them an antagonist effect.
A tumor usually found in the adrenal medulla that releases a mix of epinephrine and norepinephrine. Symptoms include signs of catecholamine excess, including intermittent or sustained hypertension, headaches, palpitations, and increased sweating. Dx is made on the basis of chemical assay of circulating catecholamine metabolites, especially 3-hydroxy-4-methooxymandelic acid, metanephrine, and normetanephrine. Treatment is the use of Alpha-Receptor blocking drugs including both phenoxybenzamine and phentolamine.
Phenoxybenzamine forms a reactive ethyleneimonium intermediate that covalently binds to α receptors.
Contract smooth muscle. Given IV - cause vasodilation, due to release of NO. Different intracellular signal than Alpha 1 receptors.
Direct Acting Cholinomimetic Agonists
All are choline esters
1. Acetylcholine Both M & N
2. Carbachol Both M & N (glaucoma)
3. Methacholine M
4. Bethanochol M

All are alkaloids
1. Pilocarpine M (Sjogren's glaucoma)
2. Nicotine N (depolarizing blockade w/ any nicotinic agonist)
3. Mucarine M
Indirect Acting Cholinomimetic Agonists
Less selective, prevent breakdown of Ach. Inhibit Ach-esterase or cholinesterase.
3 main classes of Indirect Acting Cholinomimetic Agonists
1. Edrophonium
2. Carbomates (reversible-competitive)
3. Organophosphates (irreversible)
short-acting, 15 min.
poorly lipid soluble
1. Neostigmine - PO, 30 min-2hr, poorly lipid soluble
2. Physastigmine - PO, 30min - 2hr, lipid soluble
3. Pyridostigmine
1. Echothiophate: 2-7 days
2. Parathion: 7-30 days, Used in pestcides, very rapidly fatal. Give atropine or cholinesterase regenerator - Pralidoxime.
Drugs for Myasthenia Gravis
1. Edrophonium - short-acting, used to make Dx, fatigued tongue muscle, hard to speak.
2. Neostigmine & Pyridostigmine - used in TX, both long-acting.
Drugs for Glaucoma
1. Physastigmine
2. Echothiophate
Muscarinic Antagonists
Drug List
1. Atropine - bronchdilation, GI, GU
2. Scoplopamine - CNS (motion sickness)
3. Bentropine - Parkinson's
4. Ipatropium - bronchodilation (inhaler; asthma, COPD)
5. Methscapolamine - GU, GI
6. Propantheline - GI
7. Glycopyrrolate - GU
8. Oxybutnin - GU
9. Tolterodine - GU
10. Pirenzepine - GI
11. Topicamide - Mydriatic
Muscarinic Antagonist Toxicity
vision problems
unable to urinate, defecate, or spit
atropine fever - blocking due to thermaregulation - can cause death
caution - arrthymias, elderly, BPH (benign prostatic hypertrophy)
Nicotinic Antagonists
Neuromuscular blockers
1. Nondepoloarizing (competitive) - Tubocurarine (Flacid Paralysis - 30-60min)
2. Depolarizing - Succinylcholine
Selective Direct Adrenergic Agonists
1. Phenylephrine
2. Methoxamine
3. Clonidine
4. Methylnorepinephrine
5. Dobutamine
6. Dopamine
7. Terbutaline
8. Albuterol
9. Ritodrine
Non-Selective Direct Adrenergic Agonists
1. Alpha1 Alpha2 - Oxymetazoline
2. Beta1 Beta2 - Isoproterenol
3. Alpha1 Alpha2 Beta1 Beta2 - Epi
4. Alpha1 Alpha2 Beta - NE
Neuronal Adrenergic Agonists
1. Reserpine
2. Guanethidine - competes with catecholimines for uptake (ex. NE). Concentrates into vesicle and displaces NE. Can cause depletion and prevents release of NE indirectly.
Mixed Adrenergic Agonists
Ephedrine Alpha1 Alpha2 Beta1 Beta 2
(Direct and releasing Indirct)
response decreased
(resperine and guan.)
Indirect Adrenergic Agonists
1. Amphetamine
2. Tyramine
Uptake Inhibitors
1. Cocaine
2. Tricyclic Antidepressants
MAO or COMT inhibitors
1. Paragyline
2. Entacapone
Catecholiomines are synthesized
Adrenoreceptor Antagonist Drugs
Alpha Blockers
1. Phenoxybenzamine
2. Prazosin
3. Terazosin
4. Doxazosin
5. Phentolamine
6. Yohimbine
Adrenoreceptor Antagonist Drugs
Beta Blockers
1. Propranol (prototype)
2. Nadolol
3. Timolol - used in eye drops
4. Labetalol
5. Metoprolol (cardioselective)
6. Atenolol (cardioselective)
7. Esmolol (very short acting)
Alpha & Beta
8. Carvedilol
Muscarinic Toxicity
CNS stimulation
Miosis, spasm of accomadation
Increased GI & GU smooth muscle activity
Increased secretory activity
Reflex tachycardia
Nicotinic Toxicity
CNS stimulation, including conulsions followed by depression
Ganglionic stimulation and block
Neuromuscular end plate depolarization leading to fasciculations and paralysis
Ganglion Blockers
1. Hexamethomium
2. Trimethaphan
3. Mecamylamine
Substance P
Sensory neuron transmitter in ENS. Tachykinins - excitatory w/ Ach at ENS. Vasodilator via release NO.
Amphetamine used in narcolepsy.