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Ganglion – Small mass of nerve tissue containing the cell bodies of neurons
Synapse – space b/w pre & post neurons or space b/w post neuron & effector where Neurotransmitter (NT) is released
Somatic NS:
-VOLUNTARY
Autonomic NS:
-regulates activity of smooth musc, exocrine glands, cardiac tissue, certain metabolic activities
-Motor neurons go from smooth muscle & cardiac muscle (and glands) from the CNS
-INVOLUNTARY
Enteric NS:
-Neurotransmitter: NOREPINPEHRINE/NORADRENALINE
Parasynpathetic NS:
-Neurotransmitter: ACETYLCHOLINE
General Effects of PNS/SNS:
PNS: Responses are specific, rest & digest, miosis (constrict pupil), inc gi motility and salivation, inc urination and defecation,
dec heart rate, bronchoconstriction, erection
SNS: responses diffuse, fight/flight, mydriasis (dilation of pupil), dec GI motility/salivation, bronchodilate, ejaculation, opposite
of PNS
Effected Organ Adrenergic (SNS) SNS effect Cholinergic (PNS) PNS effect
receptor receptor
NT: NT:
-epinephrine -acetylcholine
(adrenaline)
-nicotine
-norepinephrine
(noradrenaline)
2 dilation
Gluconeogenesis
(A) There are muscarinic acetylcholine receptors which are located at the PNS nej, some SNS nej (sweat glands), CNS, and
autonomic ganglia.
-EFFECTS MUSCARINIC RECEPTORS: SLUDGE – SALIVATION, LACRIMATION, URINATION, DEFECATION, GI MOTILITY, ERECTION
Bronchoconstriction
Peripheral vasodilation
Miosis
(B) There are also nicotinic acetylcholine receptors which is activated by ACH and NICOTINE
-Located on autonomic ganglia (excites neurotransmission) and somatic neuromuscular junctions (activates muscule
contraction)
1 adrenergic receptors
• It’s goal is inhibition of NE release from nerve endings at pre synaptic post ganglionic neuron (negative
feedback)
1 receptor
• Located on SNS effector (cardiac muscle, vascular smooth muscle, renal cells - renin release, inc BP)
• Increased lipolysis
2 receptor
• Located on SNS effector (dilates bronchioles in lung, uterine smooth muscle and vascular smooth muscle)
Indirect agonists: stimulate release of NT, inhibit reuptake of NT, inhibit metabolism of NT
Indirect antagonists: Inhibit synthesis of NT, prevent vesicular storage of NT, inhibit release of NT
Cholinergic Agonists
Direct: bind and activate cholinergic receptors (activates PNS) [Choline esters, plant alkaloids]
CHOLINE ESTERS:
ACH and Carbachol – activate both nicotinic and muscarinic. ACH has limited clinical indications
• Lack of specificity for muscarinic subtypes, therefore have a wide range of effects on many organ systems
Bethanechol and methacholine– activates only muscarinic. Methacholine not commercially available
Bethanechol (Urecholine)
PLANT ALKALOIDS:
• Treats glaucoma: stimulate contraction of ciliary muscle fibers aqueous humor outflow Intraocular
pressure
Cevimeline (Exovac)
CHOLINESTERASE INHIBITORS:
An acetylcholinesterase inhibitor (often abbreviated AChEI) or anti-cholinesterase is a chemical or a drug that inhibits the
acetylcholinesterase enzyme from breaking down acetylcholine, thereby increasing both the level and duration of action of the
neurotransmitter acetylcholine.
MOA: Inhibit breakdown of ACH at all cholinergic synapses increase ACH concentration
Reversible vs Irreversible
Reversible agents
• Edrophonium (Enlon) - very short DOA. Used in Dx of Myasthenia gravis muscle weakness disease
• Neostigmine (Prostigmin) - Tx of Myasthenia gravis, antidote for skeletal muscle relaxants (reverse anesthesia)
• Physostigmine (Eserine) - Tx Overdoses of drugs with anticholinergic effects (i.e. atropine, TCAs)
• Pyridostigmine (Mestinon) – Tx of Myasthenia gravis
Irreversible (organophosphates)
CHOLINERGIC ANTAGONISTS
• Both types inhibit effects of PNS stimulation SM relaxes, inc HR/CO, inhibit exocrine gland secretion
ATROPINE
Ocular Effects Mydriasis & inhibit lacrimal gland for dry eyes [therapeutic effect to facilitate eye exam]
Ipratropium or tiotropium
GI/Urinary Effects Relax GI muscle, reduce intestinal motility, inhibit gastric acid secretion, inc urinary retention
CNS Effects Tx motion sickness by blocking cholinergic transmission, tx of parkinson’s to reduce tremor
Causes muscle relaxation and paralysis, reversed by cholinesterase inhibitors, used for surgery
Remember, physiological responses can be organized according to receptor type:
• Alpha 1: vasoconstriction and increased blood pressure and total peripheral resistance
Adrenergic Agonists
Catecholamines
Must be given parenterally (IV, IM, etc. doesn’t include GI tract due to rapid metabolization)
• Dopamine - precursor to epi, NE [cardiogenic shock, septic shock, HF, hypovolemic shock]
Inc BP (a1)
• Phenylephrine
• Albuterol [asthma]
Bronchodilation (2)
Inhibits NE release from nerve terminal of postganglionic neuron (feedback inhibition a2) and lows
BP
• Cocaine [anesthetic]
ADRENERGIC ANTAGONISTS:
Phenoxybenzamine
noncompetitive, irreversible
tx HTN episodes w/ pheochromocytoma (tumor w/in adrenal glands which secrete epi/NE)
Phentolamine
competitive, reversible
Youtube Note: because they block a2, that means NE production is inc stimulates beta 1 receptors on the heart can lead
to tachycardia and cardiac arrhythmias
-dec BP
-medicines end with -azosin -doxazosin, prazosin, terazosin, tamsulosin, alfuzosin [only for BPH because inc sensitivity for
for a1 receptors in prostate]
B1 block = dec bp, dec CO, dec renin, dec aqueous humor secretion
-Atenolol, Metoprolol
-carvedilol, labetalol [HTN for both, CHF for former] {blocks beta and alpha 1}