Acetylcholinesterase Agents SUMMARY

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Acetylcholinesterase Agents
AChE distribution: CNS and PNS
BuChE (pseudocholinesterase) distribution: plasma and liver. Effects of antiAChE are AChE inhibitin> causes accumulation of AChE.
Vamos lembrar da neutransmissao colinergica!
Choline is transported from the extracellular fluid into the cytoplasm of the cholinergic neuron by an energy-dependent carrier system that cotransports sodium. Choline acetyltransferase catalyzes the reaction of choline with acetyl coenzyme A (CoA) to form ACh (an ester) in the cytosol. > The uptake of choline is the rate-limiting step in ACh synthesis <
ACh is packaged and stored into presynaptic vesicles by an active transport process coupled to the efflux of protons. The mature vesicle contains not only ACh but also adenosine triphosphate (ATP) and proteoglycan.
When an action potential propagated by voltage-sensitive sodium channels arrives at a nerve ending, voltage-sensitive calcium channels on the presynaptic membrane open, causing an increase in the concentration of intracellular calcium. Elevated calcium levels promote the fusion of synaptic vesicles with the cell membrane and the release of their contents into the synaptic space.
ACh released from the synaptic vesicles diffuses across the synaptic space and binds to either of two postsynaptic receptors on the target cell, to presynaptic receptors in the membrane of the neuron that released the ACh, or to other targeted presynaptic receptors. The postsynaptic cholinergic receptors on the surface of the effector organs are divided into two classes: muscarinic and nicotinic. Binding to a receptor leads to a biologic response within the cell, such as the initiation of a nerve impulse in a postganglionic fiber or activation of specific enzymes in effector cells, as mediated by second-messenger molecules.
Neuromuscular Junctions
Nerve action potential X tetrodotoxin; batrachotoxin; local anesthetics 
Vesicular Ach release X hemicholinium; botulinus toxin; pricaine’ Mg; lack of Ca. > excess of Ca
Depolarization (channel Na/K) X curare alkaloids; snake alpha toxins. --- depolarization & phase 2 block
Hydrolysis of Ach by cholinesterase X cholinesterases inhibitors
Muscle action potential X quinine tetrodotoxin; > Ca veratridine
Spread f excitation in muscle 
Muscle contraction X metabolic poisons; lack of Ca; procaine; dantrolene
CNS: many cholinergic synapses; both nicotinic and muscarinic receptors; drugs affecting CNS must cross BBB
AChE-Inhibitors
Stimulation of muscarinic receptors at autonomic neuroeffector junctions
Stimulation of autonomic ganglia via nicotinic receptors
Stimulation os skeletal muscle at neuromuscular junction via nicotinic receptors
Stimulation of CNS via central cholinergic receptors
Respiratory failure can be caused by neuromuscular paralysis and CNS depression
RECEPTORES
- Receptor GPCR (ligado a Gq – IP3 e cálcio);
- Autônomo Parassimpático;
- Inervação Colinérgica VISCERAL;
	M1
	M2
	M3
	M4
	M5
	Gq (IP3/CÁLCIO)
	Gi
(↓ cAMP)
	Gq (IP3/CÁLCIO)
	Gi
(↓ cAMP)
	Gq (IP3/CÁLCIO)
M1: 
	
LOCALIZAÇÃO
	- Glândula Gástrica;
- Córtex Cerebral
	
RESPOSTA CELULAR
	↑ IP3;
↑DAG (Diacilglicerol)
	
RESPOSTA FUNCIONAL
	- Secreção Gástrica;
- Excitação SNC (memória?)
	
AGONISTAS
	- Acetilcolina;
- Carbacol
	
ANTAGONISTAS
	
- Atropina
M2:
	
LOCALIZAÇÃO
	
- Coração
	
RESPOSTA CELULAR
	
↓ cAMP
	
RESPOSTA FUNCIONAL
	- Inibição Cardíaca;
- Inibição efeitos muscarínicos Centrais (tremor e Hipotermia)
	
AGONISTAS
	- Acetilcolina;
- Carbacol
	
ANTAGONISTAS
	- Atropina
M3:
	
LOCALIZAÇÃO
	- Glândulas Salivares e Gástricas;
- Musculatura TGI, olhos, brônquios;
- Veias: endotélio
	 
RESPOSTA CELULAR
	
↑ IP3;
	
RESPOSTA FUNCIONAL
	- Secreção salivar e Gástrica;
- Contração musculatura TGI;
- Acomodação Ocular
- Vasodilatação
	
AGONISTAS
	- Acetilcolina;
- Carbacol
	
ANTAGONISTAS
	- Atropina
- Ipratrópio
Ações:
- Secreção gástrica;
- Secreção salivar;
- Contração do músculo gástrico;
- Acomodação ocular;
- Vasodilatação
- Antiespasmótico: Escopolamina (Buscopan), diminui a cotração involuntária do músculo liso uterino – NÃO É ANALGÉSICO, não tira dor, diminui contração;
Therapeutic Agent Drug Classes
Alcohol: binds reversible to AChE
Carbamates: binds reversible; formation of caramoylated enzyme; inhibition lasts hours
Organophosphates: binds reversible.
ACh Hydrolysis: 
ACh association with enzyme site
Tetrahedral transition state
Acetyl enzyme conjugate formed > choline release
Hydrolysis generates free enzyme and acetate
Ach -----------AChE----------> Colina + Acetato
A colina produzida na degradação da acetilcolina é recaptada pela varicosidade colinérgica, onde será reutilizada para síntese de mais acetilcolina
Exemples AchE inhibitors:
** presence of a quartenary ammonium group causes membrane permeability, GI absorption, skin penetration, crossing BBB. Confers some direct nicotinic agonist activity > causes increasing of ACh 
Myasthenia Gravis > neostigmine, pyridostigmine, edrophonium
Alzheimer > tacrine, donepeil,rivastigmine, galantamine
Atropine intoxication > physostigmine
Glaucoma
Atony of intestinal tract and urinary bladder > neostigmine (increases GI mobility; contraindication to organic bstruction)
Nerve Gases/Nerve Agents
Organophosphate AchE-inhibitors: G-series: non persistent, gases (Tabun > WW1; Sarin > as munition; Soman); V-series: persistent agents, oily, skin absorption (VX, VE, VG, VM, VR)
Toxic effects of nerve gases/nerve agents: muscarinic & nicotinic receptor stimulation. 1st eye & respiratory effects (muscarinics) > congestion, lacrimation, rhinorrhea, impaired vision, bronchospasm. Skeletal muscle (nicotinic) > weakness, paralysis. Cardiovascular (muscarinic, but some adrenergic too) > bradycardia, hypotension. GI trac and bladder. Sweting (sympathetic).
Protection & treatment: protective suit chemical. Atropine > dose high enough to block CNS muscarinic receptors *doesn’t block nicotinic effects from ACHE-I. Pralidoxime > bind organophosphates-inactivated AChE.
** Presence of tertiary amines & more lipophilic agents: well absorbed from GI tract; affect both PNS & CNS; long term storage on lipids; easily penetrate skin; can penetrate lungs.
Non-Therapeutic Uses
Warfare
Insecticides 
Treatment of toxic effects
Atropine: dose high enough to block CNS muscarinic receptors *doesn’t block nicotinic effects from ACHE-I
Pralidoxime: can regenerate enzyme activity, most at neuromuscular junction.
Emerging Contaminants: any synthetic or naturally occurring chemical or any microorganism that isn’t commonly monitored in the environment but has the potential to enter the environment and cause known or suspected adverse ecological and/or human health effects.
** Pharmaceuticals & Personal Care Products (PPCPs); chemicals from industry; agricultural chemicals (pesticides, insecticides); pathongens.
Muscarinic Receptor Antagonists
1.Atropina
- Atropa belladona;
Ações:
- Inibe secreções;
- Efeitos sobre a frequência cardíaca (taquicardia);
- Efeitos Oculares (midríase);
- Efeitos sobre o Trato Gastrointestinal (inibição da motilidade);
- Efeitos sobre a Musculatura Lisa (relaxamento da musculatura das vias brônquicas, urinárias e biliares);
Therapeutic Uses
1.Cardiovascular:
- Tratamento de bradicardia sinusal (após infarto do miocárdio) – Atropina IV;
2.Neurológico:
- Prevenção da cinetose (enjoo por movimento) - Escopolamina VO;
3.Respiratório:
- Asma (broncodilatação) - Ipratrópio/Atrovet inalação;
- Pré-anestésicos (inibição de secreções, ex: salivar em procedimentos cirúrgicos, evitar engasgamento) – Atropina e hiosciamina (escolomanina) IV;
4.GastroIntestinais:
- Antiespasmóticos (relaxamento contração involuntária da musculatura lisa) – Escopolamina (Buscopan);
- Suprimir a secreção de HCl.
____________________________
Anticholinergics > 4 ammonium MA: iprattopium, umeclidinium,trospium, tiotropium, scopolamine methylbromide, homatropine methylbromide.
	Atropine
	Scopolamine
	+ potent on hear & intestine
	+ potent on iris, ciliary muscle, secretory glands
	Doesn’t depress CNS at clinical doses
	CNS depress at clinical doses > reduced REM sleep
	At toxic doses > stimulation
	At toxic doses > stimulation
- Escopolamina: antiespasmótico. Bloqueio dos receptores parassimpáticos, diminuindo a contração involuntária da musculatura;
- Escopolamina + Dipirona (Analgésico e anti-térmico). Além da ação antiespasmótica, com a associação a dipirona, faz com que haja a ação analgésica.
- Fenoterol (Berotec): Atua como agonista no Sist. Simpático. Broncodilatação;
- Ipratrópio (Atrovent): Atua como antagonista no Sist. Parassimpático. Broncodilatação;
- Ópio: beladona (Atropa belladona) – alcaloide isoquinolínico. Atua no Parassimpático;
Sympathomimetic
Peripheral effects
- Controle da Pressão arterial;
- Motilidade e secreção Gastrointestinaal;
- Esvaziamento da bexiga urinaria;
- Sudorese;
- Controle da temperatura corporal;
- Motilidade da musculatura lisa visceral.
Metabolic effects
- increased glycogenolysis > quebra do glucagon 
- increased gluconeogenesis > formacao de glucagon
- increased lipolysis > quebra de lipidios
Endocrine effects
Modulation of renine secretion
Modulation of pancreatic secretions
Secretion of anterior pituirary (dopamine)
CNS effects
Decreased appetite
Increased wakefulness
> Sist. Simpático: Noradrenalina receptores alfa e beta;
> Os medicamentos normalmente atuam sobre as fibras pós-ganglionares, pois se atuassem sobre o pré-ganglionar, o medicamento causaria o comprometimento de todo o sistema.
Catecholamines’ receptors
- Epinephrine (EP): alpha & beta
- NE: alpha & beta1
- Isoproterenol: beta
- Dopamine: dopamine, alpha & beta1
- Dobutamine: beta1, alpha & beta2
> Epinephrine low dose response: due beta stimulation (tachycardia & hypotension)
> Epinephrine high dose response: both alpha & beta stimulation (tachycardia, + inotropism, increased peripheral resistance) 
* Inotrope is an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction.
> Cardiac Efficiency (E): work done/oxygen uptake
Decreased efficiency since EP increases oxygen uptake.
Increased angina w/ insufficiency coronary circulation
Alpha Agonists in Glaucoma: 
Alpha 1 agonism: cilliary vessel vasoconstriction > reduces aqueous humor formation
Alpha 2 agonism: cilliary body > reduces aqueous humor formation
EP uses:
- Respiratory distress as aerosol
- Prolong local anesthetic action
- Topical hemostatic
- Cardiac arrest emergencies directly on heart
- Topical in open angle glaucoma
ADR + Beta Beta2: Broncodilatação
ADR + Beta Beta1: Aumento Freq. Cardíaca e Contração
- Asma: tratamento de emergência;
- Choque Anaflático;
- Parada Cardíaca;
- Choque Cardiogênico (agonista Beta1 – dobutamina).
EP Precautions
- increased susceptibility to pressor effects in hypertensive/hyperthyroid patients
- Angina
NE Effects
Less alpha potency than EP
Decreased renal/hepatic/muscle blood flow
Increased MABP (Mean Arterial Blood Pressure)
Reflex bradycardia
Alpha Agonist Uses
Hypotension
Local vasoconstriction
Nasal decongestion
Paroxysmal atrial tachycardia
NE Precautions
Tissue necrosis due to alpha stimulation
Hyperthyroidism
Sensitization of myocardium
Contract od gravid uterus
Isoproterenol effects
Vascular & nonvascular smooth muscle beta 2 stimulation
Hyperglycemia, FFA release
Cardiac stimulation
Bronchodilation
> Dopamine low dose effects: increases renal blood flow, glomerular filtration & sodium excretion
> Moderate dose effects (dopamine agonist + beta1 + indirect actiong sympathomimetic action): increased cardiac output, systolic BP, coronary blood flow
> High dose effects (dopamine agonist + beta1 + indirect alpha): increased peripheral resistance, renal vasoconstriction 
Dopamine use & adverse effects
Shock by continuous infusion
Increased BF to kidney & enhance glomerular filtration
Overdose: similar to sympathetic stimulation
Nausea, hypertension, arrhythmia
Dobutamine effects
At high doses resembles isoproterenol
Slight alpha & beta 2
Why is better than other catecholamines? Less tachycardia, increase in systolic BP, less effect on oxygen demand, no decreases in cardiac efficiency. 
Uses:
Shock w/ oliguria
Adverse effects: 
Cardiac arrhythmia
Tachycardia 
Comparison of NE, EP & ISO
Arterial smooth muscle: EP > NE >>> ISO
Bronchial smooth muscle: ISO > EP >>> NE
Cardiac inotropism: ISO > EP = NE
Comparison of NE, EP & ISO w/ & w/o Antagonists
Arterial smooth muscle: NE = NE + propranolol >>> NE + phentolamine
Bronchial smooth muscle: ISO = ISO + phentolamine >>> ISO + propranolol
Cardiac inotropism: -NE = NE + phentolamine >>> NE + propranolol
Denervation & Indirect Acting Sympathomimetics (IAS): Response to IAS is diminished or abolished
Adrenergic Neuron Blocker & Sympathomimetic: slight response increase to catecholamine due to postjunctional receptor upregulation; IAS response is reduced or abolished; IAS requires intact neuron to produce response
Reuptake inhibitor: pretreatment increases catecholamine agonist response since neuronal reuptake is impaired; decreases/abolishes response to IAS since neuronal uptake is blocked.
Uses of beta2 agonist: bronchodilation; premature labor
Overactive Bladder
> Oral anti-muscarinic drugs (oxybutynin, tolterodine, feosterodine…)
______________________________________________________________
Adrenergic Blocking Agents
Adrenergic Receptor Antagonists
- Non selective alpha & beta antagonists
- Alpha 1 & 2 antagonists
- Beta 1 antagonists
- combined alpha/beta antagonists
 Adrenergic Neuron Blockers
- Alpha 2 agonists
- Tyrosine hydroxylase inhibitors
- Intraneuronal storage inhibitors
- Inhibitors of NE release
- False neurotransmitter
- Chemical sympahtectomy agents
Adrenergic Blocking Agents Effects Spectrum 
Postural hypotension
Increased GI motility
Increased Na retention & blood volume
Nasal stuffiness
Extrapyramidal symptoms
Impaired ejaculation
Depression/sedation
> Non selective alpha antagonists: phenoxybenzamine, phentolamine, tolazoline, ergot alkaloids.
> Selective alpha antagonists: alpha 1: prazosin, terazosin, doxazosin; alpha 2: yohimbine
> Antagonists are + effective vs exogenous agonists
> Effect produced depends upon magnitude of tone
> Differences in pre & post junctional receptor blockage
Phenoxybenzamine: 
- prototype alpha blocker;
Usos Terapêuticos:
- Feocromocitoma (tumor na adrenal)
- (+) Atenolol (beta-bloqueador).
> Effects: no BP effects, except in hypovolemia or upright posture; EP reversal; prejunctional alpha antagonists.
> Precautions & adverse effects: hypovolemia; exaggerates vascular relaxation; mutagen
Tolazoline & Phentolamine
- Transient competitive antagonism
- Mixed effects: sympathetics, cholinergic & histaminergic
- Direct vasodilation
> Adverse effects & precautions of phetolamine: reflex tachycardia; GI stimulation; exacerbation of peptic ulcer; coronary artery disease. Taquicardia (bloqueio Alfa2 e reflexo barorreceptores); Reversão da Adrenalina.
Selective alpha 1 antagonists: decrease peripheral resitance & venous return to heart; negligible tachycardia. 
Ergot Alkaloid MOA: partial agonists; alpha antagonism.
Usos Terapêuticos:
- Enxaqueca > Dihydroergot alkaloid
- Hemorragia pós-parto.
Efeitos Adversos:
- Alucinações;
- Grangena.
Ergonovine: poewrful oxytocic; stimulates uterus postpartum contraction; partial agonist at alpha receptors > partial agonist at dopamine & serotonin receptors.
Yohimbine: increases NE releases & HR & BP due to alpha 2 antagonism’ increased antidiuretic hormone release from pituitary. 
- Aumento do Fluxo simpático;
- Afla2 pré-sináptico= mecanismo auto inibitório
Alfa2 + Gi corpo cavernoso peniano (normal)
Alfa2 + Gi + Antagonista Alfa2 (ioimbina) é excitatório, estimula a liberação de óxido nítrico, que é uma substância vasodilatadora, oferencendo maior fluxo sanguíneos - causando ereção.
- NÃO SIMMPATOLÍTICO
Non selective Beta Antagonists
Propranolol, timolol, nadolol, pindolo;, carvedilol.
Timolol: glaucoma; decreases intraocular pressure:, reduces formation of intraocular fluid.
Timolol (x) Beta (x) Gs (o) Gi (x) Adenilato ciclase (x) cAMP ↓ Humor aquoso ↓ Pressão intraocular;
Nadolol: long half-life; low lipid solubility; low brain [] compared w/ propranolol. Used hypertension, ischemic heart disease, arrhythimias. DOESN’T discontinue abrupty; pulmonary effects in asthamatics. 
Metoprolol: beta 1 selective; less pulmonary effects; 
Labetalol: competitive antagonists at alpha & beta receptors. 4 isomers. Inhibition on NE reuptake. 
Usos Terapêuticos:
- Hipertensão crônica
- Emergências hipertensivas;
- Feocromocitoma (tumor na adrenal, alta secreção de NA)
Efeitos Adversos:
- Hipotensão postural;#
- Sonolência.#
# ambos pelo antagonismo em Alfa.
Carvedilol: produces vasodilation; decreases PV resistance; active metabolities
Esmolol: used for tachycardia after cardiac surgery.
Nebivolol: poor metabolizers/renal disease or larger doses lose selectively.
MOA > decreasesd HR, - inotropism; decreasesd PNS symp tone from CNS; decreased renin activity; vasodilation’ decreased PS resistance.
Propranolol: 
- Bloqueio Beta1 = Beta2
Usos Terapêuticos:
- Angina;
- Hipertensão;
- Arritmias;
- Tremores;
- Taquicardia;
Efeitos Adversos:
- Sedação;
- Distúrbios do sono;
- Distúrbios metabólicos: Diminuição glicogenólise (receptores Beta2 no fígado, FUGA! Maior necessidade de glicose), diminuindo nível glicose, aumento de glicogênio;
- Bronococonstrição
- O PROPANOLOL pode ser usado como medicamento para Hipertensão Leve e Moderada, com ação em Beta1.
- Propanolol: antagonismo em Beta1 e Beta2 pulmão, utilizado para quem sofre de nervosismo; ação em Beta2 vascular, diminuiu o rubor (vermelhidão da face - vasodilatação), pois provoca vasoconstrição.
- Propanolol: Enxaqueca (vasodilatação); agindo em Beta2 vascular, causando vasoconstrição, diminuindo os sintomas da enxaqueca;
Non selective beta blockers effects:
- Antagonismo em Beta = ↓cronotrópico e ↓inotrópico;
- Atividade Anti-hipertensiva:
* Sem efeitos em indivíduos ormais;
* Redução do Débito Cardíaco;
* Diminuição na Liberação de Reina (rins);
* Bloqueio Beta (pré-sináptico).
- Broncoconstrição (antagonismo em Beta2);
- Enxaqueca;
- Abstinência ao álcool (↓ ansiedade e ↓tremor);
- Tremores de ansiedade.
USES: hypertension, glaucoma, angina.
Adrenergic Neuron Blockers
Guanethidine: taken into adrenergic neuron; inhibitors response to symp stmulation & response to IAS; sensitizes effectores to catecholamines; reduces NE release; no CNS/adrenal medulla effects.
> long term effects: decreases MABP, bradycardia, decreased cardiac ouput.
> toxicity & precatutions: postural hypotension; increases GI motility; inhibits ejaculation
Bretylium
Reserpine: central & peripheral actions; acts at storage vesicles to inhbiti NE & dopamine storage > deamination. Deplets biogeninc amines sucha as NE, dopamine & serotonin; decreases brain catecholamines
> toxicity & precautions: sedation; psychotic depression; breast cancer?; wight gain; increases GI moitily, increases GI secretions
> Alpha methyl p Tyrosine: pheochromocytoma; indication to surgery preparation.
Ganglionic Blockers
Chantix
Not a ganglionic blocker
Classified as nicotinic receptor partial agonist
Complex nicotinic receptor subtype profile
Partial agonist at a4 b2 nicotine receptor subtypes (see previous)
Full agonist at a7 nicotine receptor subtypes (see previous)
Weak or partial agonist at other nicotinic receptor subtypes
Crosses the blood brain barrier
Used in treating tobacco smokers for nicotine addiction
Nausea is a common side effect 
Shows clinical efficacy, but has black box warning
Problems with changes in mood and behavior including depression, suicidal thoughts, and suicide
Ganglionic Neurotransmission
ACh released from preganglionic neurons that have cell bodies in the CNS
Activation of nicotinic Nn receptors depolarizes postganglionic neurons
Nn receptor activation elicits excitatory post synaptic potential (EPSP)
	 [Note: in muscle we would call this an end-plate potential (EPP)]
If threshold is reached an action potential in the postganglionic neuron is initiated
Ganglionic communication is complex:
> initial EPSP elicited by Nn receptor activation; Nicotine is an agonist
> secondary events following Nn activation are not mediated by Nn receptors:
> slower inhibitory post synaptic potential follows (IPSP) mediated by M2 receptor activation
> secondary slow EPSP follows the IPSP mediated by M1 receptor activation by ACh
> later, slow EPSP follows the above slow EPSP that is mediated by many different neuropeptides
Ganglionic Stimulants
stimulate cholinergic receptors on autonomic ganglia
nicotine mimics the initial EPSP seen in ganglionic neurotransmission; blocked by ganglionic nicotinic-receptor antagonists
muscarinic-receptor agonists mimic delayed excitatory effects; blocked by atropine
nicotine, lobeline are natural alkaloids
lobeline has mixed agonist-antagonist properties at nicotinic receptors and other properties
nicotine initially stimulates then elicits blocking actions (more later)
TMA and DMPP stimulate, but have less blocking action
limited therapeutic use now
Ganglionic blockers
Hexamethonium blocks the channel associated with the Nn receptor and blocks ganglionic transmission.
Trimethaphan competes with ACh for the Ach binding site on the Nn receptor and blocks ganglionic transmission.
Mecamylamine binds the ACh binding site on the Nn receptor and blocks ganglionic transmission. In contrast to hexamethonium and trimehtaphan, significant amounts of mecamylamine get through the B.B.B. and enter the CNS. Mecamylamine can affect the “rewarding effects” of tobacco smoking resulting from nicotine.
Typical effects in patients with normal cardiovascular function:
vasodilation
decreased blood pressure & postural hypotension
often mild tachycardia and reduced cardiac output
atony in GI tract and bladder
anhidrosis
xerostomia
cycloplegia
Nicotine, a Nn and Nm agonist
complex effects on autonomic ganglia via Nn
opposing effects from Nn activation: 
> receptor stimulation and ganglionic stimulation
> depolarization block of neurotransmission
> receptor desensitization (even after some repolarization)
Examples:
Increases HR due to stimulation of sympathetic ganglia
Increases HR due to paralysis of parasympathetic ganglia
Decreases HR due to paralysis of sympathetic ganglia
Decreases HR due to stimulation of parasympathetic ganglia
High nicotine dose: effects on neuromuscular junction similar to effects on ganglia
Stimulant phase quickly followed by paralysis
Receptor desensitization
Ganglionic Blockers as Therapeutic Agents
Used in the past to control hypertension, but side-effect profile intolerable
Formerly used for treating acute hypertensive crisis
Alternative drugs used to treat acute hypertensive crisis
Alternative drugs used for controlling blood pressure during surgical procedures
Pre-ganglionic neuron
Pos-ganglionic neuron
N - Receptor
ACh
ACh
M - Receptor
Pre-ganglionic neuron
Pos-ganglionic neuron
Neuroeffector junction
ACh
N - Receptor
NE
Adrenergic Receptor
Neuroeffector junction
Cholinergic
Cholinergic
Cholinergic
Adrenergic
ACh
N - Receptor
Myoneural/Neuromuscular junction
Cholinergic
Motor neuron
Autonomic Nervous System
Parasympathetic
Involuntary
Autonomic Nervous System
Sympathetic
Involuntary
Somatic Nervous System
Voluntary
CNS > complex of nerve tissues that controls theactivities of the body (brain/spinal cord)
PNS > nervous system outside of the brain and spinal cord