Transcript
Pharmacology- ICourse CodeNumber 201311
Prof. Dr. Abdulrahim Abu Jayyab
Basic Principles of Pharmacology
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Introduction to Pharmacology Pharmacology: is derived from the Greek terms Pharmacon which means a drug or medicine and
logo which means learning, Knowledge or science.
Definition of Pharmacology: Study of the manner in which the function of living systems is
affected by chemical agents. Other term pharmacology the effect of a drug (chemical) on the body
(living system).Drug is derived from the French word Drogue which means dry herb.Pharmacotherapy: term very close to Pharmacology and in fact practical application of Pharmacology- causal (it is possible to treat the cause of disease: antimicrobial therapy, substitution of some enzymes, hormones ..)
Pharmacodynamics : mechanisms of the effects of drug on the body which deal with 1. Actions2. Mechanism of action3. Uses4. Dose5. Frequently of administration6. Side effects7. Contraindications
•Pharmacokinetics: the way the body affects the drug during (with) time (absorption, distribution, metabolism, excretion) that means it deals with 1.Route of administration2.Absorption3.Distribution (2,3,4,5) ADME4.Metabolism5.Elimination 6.Excretion
General pharmacology: describes general actions which determine the action and activity of a drugSpecial pharmacology: description of individual drugs and therapeutic groups of drugs - Molecular pharmacology concerns with the effects of drugs from the point of view of their molecular action- Pharmacogenetics deals eith the genetic aspects of the action
- Clinical pharmacology which covers the clinical use and trial of drugs- Toxicology The Area of pharmacology that deals with the adverse (reaction) effect of chemicals and drugs on biological systems. On other term toxicology is the study of adverse reactions of chemicals or physical agent on living organisms.
Definition of Drug : Any substance that brings about a change in biologic function through its chemical action. Alters state in the body in other term Drug: That is a substance that produced by various sources which when administered into the body restores the normal body function that have disturbed by a disease.
Drug Sources:-•Plants e.g. alkaloids, morphine, digoxin quinine and pilocarpine.•Animal: insulin, vitamins, sera, vaccines and thyroxine.•Mineral e.g. magnesium, iron, Zn sulphate Ca+2 and selnum.•Synthetic eg. Aspirin, chloroquine, sulphonamides and procaine.•Biosynthesis microorganism, antibiotics e.g. Penicillin, streptomycin and ….•Genetic engineering (recombinant DNA technology) insulin, growth hormone, interferone and erthropoeitin.
ROUTES OF DRUG ADMINISTRATION
Absorption of Drugs:Absorption is the transfer of drug from it site of administration to the blood stream. The rate and efficiency of absorption depend on the route of administration I.V. administration absorption is complete, that is the total dose of drug reaches the systemic circulation. Drug administration by other routes may result in only partial absorption. For example, oral administration requires that a drug dissolve in the gastrointestinal fluid and then penetrate the epithelial cells of the intestinal mucosa
Transport of drug from the GI tract drugs may be absorbed from the GI tract by either passive diffusion or active transport.•Passive diffusion: NO energy is required and diffusion means drugs moves from region of high concentration to a region of low concentration. Diffusion does not involve a carrier. Lipid-soluble drugs readily move across most biological membranes where as water soluble drugs penetrate the cell membrane through aqueous channels.•Active transport: that is required energy and involve specific carrier proteins. Active transport is energy dependent and is driven by the hydrolysis of ATP. It is capable of moving drugs against a concentration gradient.
Fate of Drugs:-Drug absorption into general circulation•binding to the receptors (reversible)•binding to tissues (fats)•binding to plasma protein•metabolism•liver b)kidney c) intestine d) blood e) lungs of tissues•Eliminationa) nasal secretions b) milk c) urine d) tears e) stool f) sweat g) saliva
h) exhaled air
Chemical signaling between cells:-1. Hormones
Specialized endocrine cells secrete hormones into the blood stream. Where they travel throughout the body
exerting effect on target cells distributed in the body.2. Neurotransmitters
Each neurons release certain chemical signals called neurotransmitters from the nerve terminals. These
substances rapidly diffuse across gap (synapse) between nerves endings and combine with specific
receptors.3. Local mediator
Most cells in the body secrete chemicals that act locally. These chemicals signals are rapidly destroyed or
removed. They do not enter the blood and are not distributed throughout the body. Histamines and
prostaglandins are examples of local mediators
Receptor: Specific molecule that drug may interact with that plays a regulatory function roleNature of ReceptorsThese are macromolecules composed of :ProteinsGlycoproteinsPhospholipids
In anther means Receptor binds to specific drugs. For each drug there
may be more than one specific binding site depending upon the organ
involved.Binding of drugs to receptors by
involve:•H-bond
•Ionic bond•Vander Waals bond•Dipole-dipole bond
•Covalent bond which is the strongestGenerally, we select drug that binds
with other than types of covalent binding.
Membrane receptorsAll neurotransmitters and most hormones and local mediators are too hydrophilic to penetrate the lipid bilayer of target-cell plasma membrane. Instead, their signal is mediated by binding to specific receptors on the cell surface.
Types of neurotransmittersAlthough over 50 chemical signal molecules in the nervous system have been tentatively identified, only 6 signal compounds, NE, E, actylcholine, dopamine, seretonin, histamine, and gama amine butyric-acid – are mostly commonly involved in the action of therapeutically useful drugs, which have clinical applications
Types of Receptors
Cholinergic receptorsa) Muscarinic receptors (Atropine-sensitive) Blocked by atropine •M1, M2, M3 , M4 And M5b) Nicotine (N) receptors classified according to the blocking agent•neuronal (Nn) Etamon sensitive receptors•muscle (Nm) curare sensitive receptors
•Adrenergic receptors•Alpha-receptors classified into•Alpha 1
•Alpha2
•Beta - adrenoreceptors classified into•Beta1 adreno receptors
•Beta2 adreno receptors
•Beta3 adreno receptors
•Histaminergic receptors•H1 receptors
•H2 receptors
•H3 receptors
•H4 receptors•Serotonin receptorsThree types : a) 5-HT1
b) 5HT2
c) 5HT3
•Dopaminergic receptors•D1 receptors•D2 receptors•D3 receptors•D4 receptors•Purioreceptors•Purine (P1) receptors
•Adenosine A1
•Adenosine A2
•Purine P2 receptors
•GABA receptors•GABAa•GABAb
•Glycine receptors•Glutamic receptors•Asparate receptors
•Opioide receptors•Receptors for endocrine hormones
•Bonzadiazaphine receptors•Prostanoid receptors – five types
Drugs Also drug can be defined as the following It is any chemical substances that alters body functions by interaction at the molecular level and can be used for diagnosis, prevention or treatment of disease.According to the mode of action Drugs are divided into:•Agonist•Antiagonist•Dudlist (partial agonist)
Agonist: It is a chemical which when added to tissues produces an observable or a measurable effect.Antagonist: Is a chemical which has no an observable or a measurable effect. But block or antagonises the action of agonist.
Dulist (partial agonist): Is a chemical which has the ability to
induce an initial effect which can be observed or
measured and it also has the ability to block the action of an agonist
acting on the same receptors.
Types of Antagonists:-
1. Competitive antagonist:-It is a drug which blockage can be overcome by increasing the concentration of agonist.e.g. Hyoscine against Ach.2. Non-competitive antagonists:-It is a drug which blockade cannot be overcome by increasing the concentration of agonist.e.g. Phenoxybenzamine against NA3. Chemical antagonist:-4- Pharmacokinetics anatagonist5- Physiological antagonists or pharmacological anatagonists: It is a drug which decreases the effect of an agonist by producing an equal opposite effect.
Definition of Some Concepts
1 . Half-life of drugs (t1/2) = It is the time required for maximum level of drug concentrated to drop 50% of maximum concentration.•Continuous absorption > metabolism +Excretion•Balance between absorption and metabolism + excretion•Due to absorption < metabolism and excretion
2. Therapeutic plasma level (TPL): Concentration. Of drug which is required to
obtain an optimal effect of that drug.•For most drugs TPL is half the max.
concentration. can be obtained of the drug (i.e. at the t1/2 of drug).
•For most drugs the interval between doses (frequency of administration) is
equivalent to t1/2 of the drug.N.B. For some drugs, there is no relation between therapeutic plasma level and the
effect e.g. locally acting drug in GIT – Anti-cancer
drugs.
3 . Effective Dose 50 ED50 : It is the dose required to produce 50% of the maximum effect.4 . Lethal Dose 50 or Toxic 50 LD50: the dose that produces death in 50% of a group.5 . Therapeutic index:- It is the ratio between toxic or lethal dose 50 (TD50 or LD50) and effective dose 50 (ED50).( i.e. T.I. LD50 ) For each drug we must determine therapeutic index
ED50
The higher the therapeutic index, the safer the drug.•Therapeutic Index (T.I) of cardiac glycosides = 2 therefore not safe.•T. I of most drugs = 10, therefore is safe.•For several drugs, in comparison, conc. must be in moles and effect in % of maximum.The potent drug is that drug which produce Ed50 at lower conc. (in moles).The smaller the ED50 in moles for a certain group of drugs the more potent the drug.
Metabolism of Drugs Some drugs are unmetabolised, they are excreted unchanged (in urine or faeces)Metabolism:-•Microsomal enzymes : Mostly present in the liver•Nonmicrosomal enzymes : Present at any site of cell (cytoplasm, mitochondria, plasma)The most important microsomal enzyme is Cytochrome P-450.Microsomal enzymes can be inhibited or stimulated by certain drugs.Non Microsomal enzymes can be inhibited only by certain drugs.
If we administer drug x which is metabolised by microsomal enzymes and drug B which stimulates synthesis of metabolising enzymes. Thus, the t1/2 of drug X in present of drug B will be decreased (i.e. metabolised faster).
Factors which effect the drug t1/2 or duration:
1. Co-administration of other drugs:-e.g. a) Microsomal enzymes inducers
synthesis e.g. phenobarbitone, Rifampicin, Nicotine. These drugs decrease t1/2 of all drugs that are metabolised by microsomal enzymes. In this case, increase frequency of administration or increase the dose.
b) Microsomal enzymes inhibitors e.g. Oral contraceptives (estrogen +
progestin), chlorampehnicol, erythromycin, cimetidine, (Tagamet).
Coadministration of these drugs with other drugs t1/2 of drug that are metabolised by microsomal enzymes.
2. Health
In case of liver disease , t1/2 will be increased in those case of drugs that are metabolized in the liver.
In renal disease t1/2 will be increased in case of drugs that
are excreted unchanged in the urine.
2. AgePersons who are considered are:-Newborn the quantity of metabolizing enzymes is low therefore t1/2 is high.Children and adults metabolizing enzymes activity is similar between children and adult.Elderly the activity of enzymes is low therefore t1/2 is high.
•Genetical factors:-In some people, the enzyme activity is low . So, t1/2 is high and more toxicity occur. So, reduce the dose or change the drug.In others, the enzyme quantity is high. So, t1/2 is low. Therefore, the dose should be increased or should be changed the drug.
Urine PH•In take of urine acidifiers:-i.e. acidic urine occur.Renal reabsorption of non-metabolized drugs usually occur in the non-ionized form.•In presence of acid, bases will be ionized. Therefore, no reabsorption happen. Therefore, duration of action.•If a patient took a toxic dose of basic drug, the best way to induce the excretion of the drug is to acidify the urine.
Means to control urine PHTo acidify urine:- By taking 1) Ascorbic acid 2) NH4ClWhich facilities elimination of basic drugs or basic poisons To alkalinize urine administer: NaHO3. The akalinization of urine hastens the excretion of acidic drugs or acidic poisons that are excreted in urine unchanged..
Definition of some terms
1 . Tolerance:- It is decrease in effect of a certain drug after chronic administration.•The cause for the loss of activity:•The increase in metabolizing enzymes (induction)•Changes affinity of the drug to the receptorsTherefore , we should increase the dose of the drug.
2 . Tacchyphylaxis:It is tolerance on isolated tissues or organs or It is loss of drug activity or effect following rapid exposure of the tissue to a drug.Tacchyphylaxis may be due to :•Effects are probably due to release of another substance (indirect simulation)High affinity of the drug to the receptor might be due to increase in the number of the receptors
3 . Receptors:- A specific cellular site that interacts with an endogenous substance or a drug molecule and mediates that compound’s action. Receptors are located in or on the cell membranes or within the cell itself. They are affected by micromolar or nanomolar concentrations, demonstrate relative stereospecificity, and be selectively blocked by antagonists.
4 . Affinity: the ability of a chemical compound to combine with a specific receptors.5 . Efficacy:- The ability of a compound to produce a physiologic/pharmacologic response. Also referred to as intrinsic activity.
6 . PotencyThe ability of a compound to produce an effect relative to its concentration. The more potent a drug is, the less concentration (dose) required to produce a maximal effect.7 . Potentiation The process that occurs when administration of a second drug increases the effectiveness of a first drug that is minimally effective or ineffective when given alone.
8. AdditivityThe process that occurs when co-administration of two drugs causes a therapeutic effect equal to the sum of effects obtained by administration of either drug individually.9 . Synergism:The process that occurs when co-administration of two drugs causes a therapeutic effect that is greater than the sum of effects obtained by administration of either drug individually.
10 . AnaphylaxisAn acute systemic
(commonly characterized by urticaria, respiratory distress, and vascular collapse) that occurs in a previously sensitized individual after exposure to the sensitizing antigen.
Intoduction to the General mechanisms of action of
Drugs
The drug may stimulates or inhibits an organ:
•1- Stimulation: a) Contraction of smooth, cardiac or skeletal muscles
• b) Release of hormones, neurotransmitter or local mediator
2- Inhibition: a) Relaxation of smooth, cardiac or skeletal muscles
b) Inhibition of release of hormones, neurotransmitter or local mediator
The cation Ca+2+ is very important for the activity of drugs.
Sites of Ca+2 ionsa) Extracellular Ca+2
b) Intracellular 1- Mitochondria2- Sarcoplasmic reticulum3- Microsomes4- Inner side plasma membraneDrug should stimulate or inhibit
influx of Ca+2 inside cells.
Mechanisms of contraction in smooth muscles
Smooth muscles: In all muscles we have two contractile proteins (actin, myosin)Actin + Myosin Actomycin [this means shortening of muscles (contraction)] The steps are as follows:-•Ca+2 interacts with Ca+2 binding protein known as calmodulin to produce a complex called Ca-calmodulin complex.•Then this complex activates light chain myosinkinases which in presence of ATP phosphorylates myosine.•The activated myosin interact with actin to produce Actomysine contraction.
Mechanisms of contraction in cardiac muscles
In cardiac muscles there is no calmodulin
Actin + Myosin ActomycinThis reaction is controlled negatively by
Troponine (which is a calcium-binding proteins)
The importance of Ca+2 is to reliefe the inhibition effect of Troponine.
•The interaction between actin and myosin is controlled negatively by the protein
troponine. free intracellular Ca+2+ leads to
interaction between Ca+2 troponine.Therefore, formation of Actomycin
contraction.Skeletal muscles contracts like cardiac
muscles.
Drug or mediator-receptors interactions:-Drugs, neurotransmitters, hormones, or local hormone bound to their receptors that gives changes in the structure of the receptors. This process is known as receptor conformation which gives DR-Complex D + R DR ComplexThis complex might cause direct action via changes the permeability of ions such as Na+ and K+ without interference of intercellular messenger systems which usually require second messenger generation. Therefore we have to classify the receptors according to its location
Classification of the Receptors
1. Located in the membrane and directly to an ion-channel. These receptors activate the cell with a time-scale of milli-seconds, e.g. the actylcholine-nicotinic receptors.2. Located in the membrane and attached via G-protein to ion channel or an enzyme, e.g. (a) Adrenaline 2 receptors in smooth muscles activates Adenylate Cyclase. (b) Noradrenaline -receptors in smooth muscles activates phospholipase C . (c) Bradykinin in fibroblasts activates phospholipase A2. All of the above receptors attached to their specific enzymes by G-protein whereas Muscurinic receptors are coupled by G-protein to K+ channels.
3. Located in the membrane and part of the receptors as protein kinase which has integral tyrosine kinase activity, e.g. Insulin receptors and receptors of growth hormone. Also could be linked to tyrosine kinase (e.g. Cytokine receptors). These receptors usually cause slower cell stimulation with a time-scale of minutes, e.g. Insulin receptors.4. Located in the cytosol or nucleus with the Ligand-receptor Complex acting on DNA that gives inhibition of protein synthesis via inhibition expression of certain genes or transcription and translation of mediator proteins, e.g. the glucocorticoid, hydrocortisone; in the case, the activation of cell is with a time-scale of minutes to hours.
Second Messengers
IntracellularReceptor-Enzyme Systems (second messenger)Phospholipase C (PLC) and Phospholipase (D)
PLC acts on Phosphatidyl Inositol 4,5 bi-phosphate (PIP2) gives Inositol 1,4,5
triphosphate (which cause influx Ca+2 from intracellular storage site leads to
increase the level of Ca+2) and other compound called Diacylglycerol
DAG (which stimulates protein kinase).PLD acts on phosphatidyl choline (PC) to
produce phosphatidic acid (PA).
Phospholipase A2 (PLA2)This enzyme produces arachidonate which might function as second messenger in some cells. And these arachidonate are considered as prostaglandine precursors. There are 5 main prostanoid receptors on each for five natural prostanoids, PGE2, PGF2, PGD2, PGF2 and TXA2 termed as EP, IP, DP, IP, IP receptors respectively.
•Adenylyl Cyclase enzymeWhich increase the synthesis of CAMP from ATP•Guanylyl Cyclase enzyme Which increase CAMP production from GTP
Mechanism of Action of Drugs
1) Drug Mediator Actions on their Receptors:-•Drug + Receptor DR Complex•This complex interacts with G-protein which is bound to GTP to give final complex.•The final complex activates the enzyme Phospholipase C (PLC).•The activated enzyme (PLC) hydrolysis a compound called phosphatidyl inositol 4,5 bi-phosphate resulting in compound : inositol 1,4,5 triphosphate (IP3) + diacylglycerol DAG•IP3 mobilizes intercellular Ca+2 and activate Ca+2 regulated enzymes and cell process. IP3 acts directly on a calcium channel on the membrane of sarcoplasmic reticulum to release stored Ca+2 in a sense of bursts. Examples: The receptors which coupled to Diacylglycerol and Inositol triphosphate (a) 1 Adrenoreceptors (b) Cholinergic muscarinic receptors M1 &. M3•Ca+2 I nteract with Ca+2 binding protein in smooth muscles and cardiac muscles @@@@ see the mechanism action of Ca+2 in these muscles.
2- Depolarization (open of Ca+2 channels) Some drugs interact with receptors to increase influx of Na+ ions increase in electrical potential within the cell. This increase in E.P. opens membrane Ca+2 channels through which intracellular Ca+2 ion influx inside the cell : increase in intacellular level of Ca+2 ion. Such as nicotinic receptor
Modulation of Cyclic Nucleotides (cAMP, cGMP)
Drugs either decrease or increase in levels.
•Increase cAMP in smooth muscles Relaxation.
•Increase cAMP in cardiac muscles Contraction.
)
Role of cAMP in Smooth Muscles:-•D + R Complex.
•Complex then interacts with Gs protein (s: stimulatory), this protein is usually linked
to enzyme adenylyl cyclase which converts ATP into cAMP.
•Guanosine is the same thing, (guanylyl cyclase).
•cAMP activates protein kinases which in presence of ATP, phosphorylates the
protein phospholamban.•The negativelly charged phosphate ions
attract the +vely charged Ca+2 ions. …decrease in intracellular Ca+2,
relaxation. (opposite to that of contraction
Role of cAMP in Cardiac Muscles:-•Drug + Receptor Complex.•This complex interacts with Gs protein. This protein is usually linked to the enzyme adenylyl cyclase which converts ATP into cAMP.•CAMP activates protein kinases which in the presence of ATP phosphorylates calcium channels resulting of influx of extracellular Ca+2. …increase in level of free intracellular Ca+2 +ve inotropic and contraction. Such as Beta adrenergic receptors•The effect of cGMP is the same.
•Gene Transcriptioni.e. synthesis or inhibition of specific proteins.•This mechanism is specifically for corticosteroids, e.g. Cortisone, Sex hormones, Thyroxine…•The receptors are present in cytoplasm.•The drug must penetrate the cell membrane and interact with receptor.•It will take time for action (min. 1 hour)
•Blockade of some Channels•If we block K+ channels the E.P. will become less negative and make partial depolarization.•Thus, drugs induce blockade of K+ channels will lead to decrease in the intracellular –ve potential leading to relative depolarization and stimulation in muscles or heart.
•Blockade of Na+ ChannelsIon channels can be affected by
some drugs. This lead to decrease in
depolarization that cause inhibition
of cell e.g. local anesthetics which
physically block the sodium channel.
•Calcium Channel Antagonists
Which bind to specific sites in the Ca+2 Channel protein inhibiting channel opening leads to decrease in intracellular Ca+2 ions that cause inhibition.
•Chloride Channel OpeningOther agent such as Benzodiazopines bind on the receptor-channel complex of the chloride channel facilitating its opening resulting in hyperdepolarization by the neurotransmitter GABA.
•Interaction with Carrier MoleculesCarrier molecules which transport ions and small inorganic molecules into or out of cells can be affected by drugs which inhibit their transports, e.g. loop diuretics on the Na+/K+/2Cl- co-transporter in the loop of Henle.
•Inhibition of some EnzymesDrug action on enzyme is usually inhibitory, e.g.
neostigmine on acetylcholinestrase (an extracellular enzyme) The action is usually directly
•often by substrate competition •but sometimes by inactivation, e.g.
• aspirin on cyclo-oxygenase.•Some drug inhibit enzymes indirectly,• e.g. heparin inhibits the coagulation
•enzymes by speeding up• the action of a natural inhibitor,
•antithrombin III.•Some drugs can themselves develop enzyme
•activity, e.g. antistreplase.
•Some Drugs Produce their Action without Interaction with Specific Receptors•Examples: •Antacids, chelating agents,•Kaolen, pectin and tannins,
Introduction to Autonomic Pharmacology
Prof. Dr. Abdulrahim Abu Jayyab
The nervous system is divided into two anatomical divisions . Central nervous system I) Brain a) Forebrain - Cerebrum - Diencephalonsb) Cerebellum c) Brain Stem - Midbrain - - Medulla oblongata -Medulla oblongata - Pones II Spinal cord- Cervical - Thoracic - Lumber – Sacral - - -Lumbar
2- Peripheral Nervous System a) Afferent Division b) Efferent Division Efferent Nervous System The Efferent Nervous System Consist of the following a) Autonomic nervous system.b) Somatic nervous system
Somatic nervous system •One motor neuron extends from theCNS to skeletal muscle•Axons are well myelinated, conduct impulses rapidlyControl voluntary activity. It innervates and controls the motor function of the body. It consists of long neurons originated or starts from the spinal cord and directly innervated skeletal muscles.
Autonomic nervous system
Other names a) Visceral b) Vegetative c) Involuntary
The Autonomic Nervous System A system of motor neurons
•Innervates smooth muscle •Cardiac muscle, •GlandsRegulates -Visceral functions-Heart rate- Blood pressure- Digestion, - Urination
Function of ANS: - Therefore, we can say in other term regulates activity of structures not under voluntary control a) Smooth muscle b) Cardiac muscle c) Secretory glands
III. Structural arrangements a) Connections — 2 neurons - 1 Neuronal fiber leaving brainstem and spinal cord synapses outside the CNS at a ganglion -- preganglionic neuron 1) Second neuron impacts on effectors organ -- postganglionic neuron b) Two divisions in ANS 1.based on differences in a- Anatomy b- Function
Can be further divided into two parts:-a) Sympathetic.b ) Parasympatheticic .
I- sympathetic (thoracolumbar) division a) Fibers originate in the thoracic and lumbar regions (T1-L3) of the spinal cord b) Ganglia are located near the spinal cord (distant from effectors organ) c) Other than a second neuron, preganglionic neurons innervate the adrenal medulla which is embryologically and anatomically analogous to other sympathetic ganglia d) One preganglionic neuron may act on many postganglionic neurons (up to1:20) e) Diffuse distribution pattern leads to widespread massive responses1- Desirable if organism is confronted with a sudden emergency (e.g. pain, asphyxia, strong emotions) 2- Fight or flight” response
II- parasympathetic (craniosacral) division a). Fibers originate in tectal region (Cranial) of the brain stem (oculomotor [III], facial[VII], glossopharyngeal [IX] and vagus [X]) and sacral segments (S2-S4) of the spinal cord b) Ganglia are located near the end effectors organs (distant from spinal cord) c) Generally 1 preganglionic:1 postganglionic neuron d) Discrete distribution leads to fine and limited responses e) Functionally important in protection, conservation and restoration of bodily resources
III. Innervations
a) Some tissues receive only parasympathetic innervations 1 - Parotid gland 2- Lachrymal gland 3- Nasopharyngeal glands
b) Some tissues receive only sympathetic innervations 1) Sweat glands 2) Adrenal medulla 3) Piloerectors 4) Most blood vessels
c) Some tissues are innervated by both 1) Salivary glands 2) Heart 3) Lungs (bronchial muscle) 4) Abdominal and pelvic viscera
d) Effect of specific drugs on organs depends on relative degree of innervations Characteristic Sympathetic ParasympatheticSpinal Cord Origin Thoracic-Lumbar Cranial-Sacral Length of Postganglionic Fiber Long Fiber ShortInnervations Diffuse(1:20) Discrete(1:1)Function Fight or Flight Minute-to- Minute Control
1) Neurotransmitter of Preganglioinc of Parasympatheticis ACh 2) Neurotransmitter of Postganglionic of Parasympathetic is Ach 3) Neurotransmitter of Preganglionic of Sympathetic is Ach4) Neurotransmitter of Postganglionic of Sympathetic is NE 5) Neurotransmitter of somatic neurons is Ach
Neurotransmitters
NeurotransmittersEndogenous chemical mediators that transmit never impulse across junction such as synapse. Neurotransmitters in the ANS are 1. Acetylcholine (ACh) 2. Norepinephrine (NE)3. Since epinephrine (Epi) is released into the circulation it is referred to as neurohormone rather than a neurotransmitter Neurons which release ACh are called cholinergic Neurons which release NE are called adrenergic
Neurotransmitters associated with the autonomic nervous system •Sympathetic division•Preganglionic neurons release ACh • postganglionic neurons release NE (ACh -->NE)• At sweat glands (ACh --> Ach)•Adrenal medulla releases Epi, NE (ACh --> Epi, b) Parasympathetic division a. Preganglionic neurons release Achb.Postganglionic neurons releaseACh (ACh->Ach)c) Caution: a. Cholinergic? Parasympathetic b. Adrenergic? Sympathetic
1- Acetylcholine It is a neurotransmitter of both sympathetic and Parasympathetic at the ganglionic synapse. Also Acetycholine is the parasympathetic neurotransmitter at the postganglionic synapse of parasympathatic.It is also a neurotransmitter of some postganglionic of sympathetic such as sweat glands ,as well as it is a neurotransmitter of somatic neurons
2-NorepinephrineIt is the neurotransmitter of sympathetic at the postgangtionic synapse . Except sweat gland and some blood vessels , which is Acetylcholine . In addition the preganglionic fiber to the adrenal medulla is acetycholine and also the somatic ( motor) nerve to Skeletal muscles .
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