Autonomic PharmacologyAdrenergic Drugs :Autonomic PharmacologyAdrenergic Drugs Recommended Reading: Adrenergic Drugs Tutorial Worth Visiting: Adrenergic ANS Formative Assessment Practice Question Set #1 Prepared and Presented by: Marc Imhotep Cray, M.D. Professor Basic Medical Sciences


Introduction :10/17/2009 IVMS 2 Introduction Distribution of adrenergic receptor subtypes and adrenergic receptor number are important factors in organ or cellular responses to adrenergic input. Adrenergic receptor type in bronchiolar smooth muscle is principally ß2: epinephrine and isoproterenol might be expected to be effective bronchodilators because of their activity at ß2 receptors. Norepinphrine is unlikely to have this same effect due to its relative lack of activity at ß2 sites.


Introduction :10/17/2009 IVMS 3 Introduction Alpha receptor dominate in the cutaneous vascular beds. Norepinephrine and epinephrine cause constriction. Isoproterenol with limited activity at alpha receptors has little effect. Both alpha and beta adrenergic receptor are present in skeletal muscle vascular beds. Alpha receptor activation causes vasoconstriction. Beta receptor activation promotes vasodilatation. Since ß2 receptors are activated at lower, physiological concentrations, vasodilation results.


Introduction (2) :10/17/2009 IVMS 4 Introduction (2) Physiological effects caused by sympathomimetcs are due not only to direct effects, but also to indirect or reflex effects. Alpha receptor agonist causes an increase in blood pressure. Carotid/aortic baroreceptors activations initiates a compensatory reflex. Sympathetic tone is reduced (decreases heart rate) Parasympathetic tone is increased (decreases heart rate) RESULTS: Blood pressure tends to return to lower levels


Categories of Action Adrenergics :10/17/2009 IVMS 5 Categories of Action Adrenergics Smooth Muscle Effects Smooth muscle activation, including activation of blood vessel vasculature (skin, kidney). Activation of glands (salivary and sweat). Smooth muscle inhibition, including inhibition of smooth muscle of the gut, bronchioles, and skeletal muscle vascular smooth muscle.  Cardiac Effects increased heart rate (positive chronotropic effect) increased contractility (positive inotropic effect) Metabolic Effects increase in rate of muscle and liver glycogenolysis increase in free-fatty acid release from fat  Endocrine Regulation/modulation of insulin, pituitary, and renin secretion  Central Nervous System Effects Respiratory stimulation CNS stimulation Appetite attenuation Presynaptic Effects Presynaptic effects: modulation of  release of norepinephrine or acetylcholine


Epinephrine :10/17/2009 IVMS 6 Epinephrine Epinephrine is a potent activator of alpha and ß adrenergic receptors Prominent Cardiovascular Effects


Epinephrine and Blood Pressure :10/17/2009 IVMS 7 Epinephrine and Blood Pressure Potent vasopressor Systolic pressure increases to a greater extent than diastolic (diastolic pressure may decrease) pulse pressure widens Epinephrine increases blood pressure by: enhancing cardiac contractility (positive inotropic effect): ß1-receptor effects increasing heart rate (positive chronotropic effect): ß1-receptor effects. vasoconstriction a1 receptor effects precapillary resistance vessels of the skin, kidney, and mucosa veins


Epinephrine and Blood Pressure (2) :10/17/2009 IVMS 8 Epinephrine and Blood Pressure (2) If epinphrine is administered relatively rapidly, the elevation of systolic pressure is likely to activate the baroreceptor system resulting in a reflex-mediated decrease in heart rate.


Epinephrine and Blood Pressure (3) :10/17/2009 IVMS 9 Epinephrine and Blood Pressure (3) A principal mechanism for arterial blood pressure control is the baroreceptor reflex. The reflex is initiated by activation of stretch receptors located in the wall of most large arteries of the chest and neck. A high density of baroreceptors is found in the wall of each internal carotid artery (just above the carotid bifurcation i.e. carotid sinus) and in the wall of the aortic arch.


Epinephrine and Blood Pressure (4) :10/17/2009 IVMS 10 Epinephrine and Blood Pressure (4) As pressure rises and especially for rapid increases in pressure: baroreceptor input to the tractus solitarius of the medulla results in inhibition of the vasoconstrictor center and excitation of the vagal (cholinergic) centers resulting in a vasodilatation of the veins and arterioles in the peripheral vascular beds. negative chronotropic and inotropic effects on the heart. (slower heart rate with reduced force of contraction)


Epinephrine and Blood Pressure (5) :10/17/2009 IVMS 11 Epinephrine and Blood Pressure (5) Adrenergic Cholinergic


Epinephrine and Blood Pressure (6) Summary :10/17/2009 IVMS 12 Epinephrine and Blood Pressure (6) Summary Blood Pressure 0.1-0.4 ug/kg/min infusion rate At lower epinephrine doses: a lessened effect on systolic pressure occurs diastolic pressures may decrease as peripheral resistance is reduced. Peripheral resistance decreased due to ß2-receptor effects


Epinephrine-Vascular Effects :10/17/2009 IVMS 13 Epinephrine-Vascular Effects Epinephrine has significant effects on smaller arteriolar and precapilliary smooth muscle. Acting through alpha1 receptors, vasocontrictor effects decrease blood flow through skin and kidney. Even at doses of epinephrine that do not affect mean blood pressure, substantially increases renal vascular resistance and reduces blood flow (40%). Renin release increases due to epinephrine effects mediated by ß2-receptors associated with juxtaglomerular cells. Acting through ß2-receptors, epinephrine causes significant vasodilation which increases blood flow through skeletal muscle and splanchnic vascular beds. If an a receptor blocker is administered, epinephrine ß2-receptor effects dominate and total peripheral resistance falls as does mean blood pressure--this phenomenon is termed "epinephrine reversal".


Epinephrine- Cardiac Effects :10/17/2009 IVMS 14 Epinephrine- Cardiac Effects Epinephrine exerts most of its effects effects on the heart through activation of ß1-adrenergic receptors. ß2- and a receptors are also present. Heart rate increases Cardiac output increases Oxygen consumption increases Direct Responses to Epinephrine increased contractility increased rate of isometric tension development increased rate of relaxation increased slope of phase-4 depolarization increased automaticity (predisposes to ectopic foci


Epinephrine- Smooth Muscle Effects :10/17/2009 IVMS 15 Epinephrine- Smooth Muscle Effects Smooth Muscle Epinephrine has variable effects on smooth muscle depending on the adrenergic subtype present.  GI smooth muscle is relaxed through activation of both alpha and ß -receptor effects.  In some cases the preexisting smooth muscle tone will influence whether contraction or relaxation results following epinephrine.


Epinephrine- Smooth Muscle Effects (2) :10/17/2009 IVMS 16 Epinephrine- Smooth Muscle Effects (2) During the last month of pregnancy, epinephrine reduces uterine tone and contractions by means of ß2-receptor activation. This effect provides the rationale for the clinical use of ß2-selective receptor agonists: ritodrine and terbutaline to delay premature labor.


Epinephrine- Pulmonary Effects :10/17/2009 IVMS 17 Epinephrine- Pulmonary Effects Epinephrine is a significant respiratory tract bronchodilator. Bronchodilation is caused by ß2-receptor activation mediated smooth muscle relaxation.  This action can antagonize other agents that promote bronchoconstriction.  ß2-receptor activation also decreases mast cell secretion. This decrease may be beneficial is management of asthma also. Pulmonary


Epinephrine- Metabolic Effects :10/17/2009 IVMS 18 Epinephrine- Metabolic Effects Pancreas Glucagon secretion: enhanced by ß adrenergic receptor activation of pancreatic islet alpha cells. Glycolysis- stimulated: by ß adrenergic receptor activation Insulin secretion: inhibited by a2 adrenergic receptor activation (dominant) Insulin secretion: enhanced by ß2 adrenergic receptor activation


Epinephrine- Metabolic Effects (2) :10/17/2009 IVMS 19 Epinephrine- Metabolic Effects (2) Liver Free fatty acids, increased: by ß adrenergic receptor activation on adipocytes--activation of triglyceride lipase


Epinephrine- Metabolic Effects (3) :10/17/2009 IVMS 20 Epinephrine- Metabolic Effects (3) Adipose Tissue Calorigenic effect (20% - 30% increase in O2 consumption): caused by triglyceride breakdown in brown adipose tissue.


Epinephrine- Metabolic Effects (4) :10/17/2009 IVMS 21 Epinephrine- Metabolic Effects (4) Electrolytes Epinephrine may activate Na+-K+ skeletal muscle pumps leading to K+ transport into cells Stress-induced epinephrine release may be responsible for relatively lower serum K+ levels preoperatively compared postoperatively. Mechanistic basis: "Preoperative hypokalemia" can be prevented by nonselective beta-adrenergic receptor antagonists {but not by cardio-selective beta1 antagonists} Possible "preoperative hypokalemia" may be associated with preoperative anxiety which promotes epinephrine release-- therapeutic decisions based on preinduction serum potassium levels to take into account this possible explanation


Norepinephrine :10/17/2009 IVMS 22 Norepinephrine Norepinephrine is the primary neurotransmitter released by postganglionic neurons of the autonomic sympathetic system Norepinephrine (Levophed) is a potent activator of a and ß1 adrenergic receptors


NE- Blood Pressure Effects :10/17/2009 IVMS 23 NE- Blood Pressure Effects Potent vasopressor Systolic and diastolic pressure increase pulse pressure widens Norepinephrine (Levophed) increases blood pressure by: vasoconstriction alpha1 receptor effects precapillary resistance vessels of the skin, kidney, and mucosa veins  Elevation of systolic pressure following norepinephrine is likely to activate the baroreceptor system resulting in a reflex-mediated decrease in heart rate.


NE- Blood Pressure Effects :10/17/2009 IVMS 24 NE- Blood Pressure Effects Blood Pressure Adaptation of Table 10-2 from: Hoffman, B.B and Lefkowitz, R.J, Catecholamines, Sympathomimetic Drugs, and Adrenergic Receptor Antagonists, In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) The McGraw-Hill Companies, Inc.,1996, pp.199-242


NE-Arterioles Effects :10/17/2009 IVMS 25 NE-Arterioles Effects Arterioles Based on Table 6-1: Lefkowitz, R.J, Hoffman, B.B and Taylor, P. Neurotransmission: The Autonomic and Somatic Motor Nervous Systems, In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,( Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp.110-111. Adrenergic Cholinergic


NE-Vascular Effects :10/17/2009 IVMS 26 NE-Vascular Effects Norepinephrine significantly increases total peripheral resistance, often inducing reflex cardiac slowing. Norepinephrine (Levophed) causes vasoconstriction in most vascular beds. Blood flow is reduced to the kidney, liver and skeletal muscle. Glomerular filtration rates are usually maintained. Norepinephrine may increase coronary blood flow (secondary to increased blood pressure and reflex activity) Norepinephrine (Levophed) may induce variant (Prinzmetal's) angina Pressor effects of norepinephrine (Levophed) are blocked by alpha-receptor blockers. ECG changes following norepinephrine (Levophed) are variable, depending on the extent of reflex vagal effects.


NE- Peripheral Circulation Effects :10/17/2009 IVMS 27 NE- Peripheral Circulation Effects Peripheral Circulation increase,             decrease 0.1-0.4 ug/kg/min IV infusion Therapeutic use: Norepinephrine may be used in treatment of shock


Dopamine :10/17/2009 IVMS 28 Dopamine Vasodilator: At low doses, dopamine (Intropin) interactions with D1 receptor subtype results in renal, mesenteric and coronary vasodilation. This effect is mediated by an increase in intracellular cyclic AMP Low doses result in enhancing glomerular filtration rates (GFR), renal blood flow, and sodium excretion. Positive inotropism: At higher doses, dopamine increase myocardial contractility through activation of ß1 adrenergic receptors Dopamine (Intropin) also promotes release of myocardial norepinephrine. Dopamine (Intropin) at these higher dosages causes an increase in systolic blood and arterial pulse pressure with little effect on diastolic pressures. Cardiovascular Effects (Dopamine) Vasopressor: At high doses dopamine (Intropin) causes vasoconstriction by activating a1 adrenergic receptors


Therapeutic use (Dopamine) :10/17/2009 IVMS 29 Therapeutic use (Dopamine) Cardiogenic and hypovolemic shock by enhancing renal perfusion despite low cardiac output Oligouria may be an indication of inadequate renal perfusion Example: dopamine may be used, in postoperative cardiopulmonary bypass patients who exhibit: low systemic blood-pressure increased atrial filling pressures low urinary output Unique among catecholamines in that Dopamine can simultaneously increase myocardial contractility glomerular filtration rate sodium excretion urine output renal blood flow


Therapeutic use (Dopamine) (2) :10/17/2009 IVMS 30 Therapeutic use (Dopamine) (2) Increased sodium excretion following dopamine may be due to inhibition of aldosterone secretion. Dopamine may inhibit renal tubular solute reabsorption(suggesting that natriuresis & diuresis may occur by different mechanisms.) Fenoldopam and dopexamine: newer drugs may be useful in treating heart failure by improving myocardial contractility


Therapeutic use (Dopamine) (3) :10/17/2009 IVMS 31 Therapeutic use (Dopamine) (3) Dopamine (Intropin) at higher doses increases myocardial contractility by ß1 - adrenergic receptor activation. Ventilation effects: -- dopamine IV infusion interferes with ventilatory responses to arterial hypoxemia Dopamine (Intropin) acts as inhibitory neurotransmitter at carotid bodies)  Consequence: Unexpected ventilation depression in patients treated with IV dopamine (Intropin) to enhance myocardial contractility


Dopexamine :10/17/2009 IVMS 32 Dopexamine Dopexamine--synthetic catecholamine Activation of dopaminergic and beta 2 receptors Slight positive inotropic effect (beta2-adrenergic agonists activity; potentiation those endogenous norepinephrine secondary to reuptake blockade) Dopexamine enhances creatinine clearance


Isoproterenol (Isuprel) :10/17/2009 IVMS 33 Isoproterenol (Isuprel) Activates ß adrenergic receptors (both ß1 - and ß2 -receptor subtypes) Has limited action at a adrenergic receptors i.v. influsion of isoproterenol results in a slight decrease in mean blood pressure with a marked drop in diastolic pressure. ß2 - adrenergic receptor-mediated reduction in peripheral resistance (reflected in the diastolic pressure effects) is primarily due to vasodilation of skeletal muscle vasculature. Renal and mesenteric vascular beds are also dilated.


Isoproterenol (Isuprel) (2) :10/17/2009 IVMS 34 Isoproterenol (Isuprel) (2) Activation of cardiac ß1 - adrenergic receptors: increased contractility and heart rate. Activation of ß2 - adrenergic receptors: Bronchial and GI smooth muscle relaxation. Isoproterenol and ß2 -selective adrenergic agonists inhibit antigen-mediated histamine release. Isoproterenol: Limited therapeutic uses: emergency settings to treat heart block or severe bradycardia management of torsades de pointes (a ventricular arrhythmia)


Isoproterenol (Isuprel) (3) :10/17/2009 IVMS 35 Isoproterenol (Isuprel) (3) management of torsades de pointes (a ventricular arrhythmia) Isoproterenol (Isuprel) adverse effects: palpitations tachycardia arrhythmias coronary insufficiency


Dobutamine (Dobutrex) :10/17/2009 IVMS 36 Dobutamine (Dobutrex) Structurally similar to dopamine (Intropin). Pharmacological effects exerted through interaction with a and ß adrenergic receptor interactions no effect on release no action through dopamine receptors Pharmacological effects are due to complex interactions of (-) and (+) enantiometic forms present in the clinically used racemate with a and ß adrenergic receptors. Dobutamine (Dobutrex) is a positive inotropic agent usually causing limited increase in heart rate. Positive inotropism is mediated through ß adrenergic receptor activation. Some peripheral a1 activity causes modest vasoconstriction, an effect opposed by dobutamines ß2 effects.


Dobutamine (Dobutrex) (2) :10/17/2009 IVMS 37 Dobutamine (Dobutrex) (2) Dobutamine (Dobutrex): Adverse Effects Significant blood pressure and heart rate increases may occur. Ventricular ectopy Increased ventricular following rate in patient with atrial fibrillation. Increased myocardial oxygen demand that may worsen post-infarct myocardial damage Dobutamine (Dobutrex): Therapeutic Use Short-term management of pump failure following surgery, during acute congestive heart failure, or post-myocardial infarction. Uncertain long-term efficacy.


ß2 Selective Adrenergic Agonists :10/17/2009 IVMS 38 ß2 Selective Adrenergic Agonists Metaproterenol (Alupent) Terbutaline (Brethine) Albuterol (Ventolin,Proventil) Ritodrine (Yutopar)


Metaproterenol (Alupent) :10/17/2009 IVMS 39 Metaproterenol (Alupent) ß2 adrenergic receptor-selective: resistant to COMT (catechol-O-methyl transferase) metabolism Less ß2 selective compared to terbutaline (Brethine) and albuterol (Ventolin,Proventil). May be used for long-term and acute treatment of bronchospasm


Terbutaline [Brethine] :10/17/2009 IVMS 40 Terbutaline [Brethine] ß2 adrenergic receptor-selective: resistant to COMT Active after oral, subcutaneous, or administration by inhalation Rapid onset of action. Used for management of chronic obstructive lung disease and for treatment of acute bronchospasm (smooth muscle bronchoconstriction), including status asthmaticus


Albuterol [Ventolin] :10/17/2009 IVMS 41 Albuterol [Ventolin] ß2 adrenergic receptor-selective Effective following inhalation or oral administration. Commonly used in chronic and acute asthma management.


Ritodrine (Yutopar) :10/17/2009 IVMS 42 Ritodrine (Yutopar) ß2 adrenergic receptor-selective: developed as a uterine relaxant May be administered by i.v. in certain patients for arresting premature labor; if successful, oral therapy may be started ß2 adrenergic receptor-selective agonists may not improve perinatal mortality and may increase maternal morbidity In women being treated for premature labor, ritodrine (Yutopar) or terbutaline (Brethine) may cause pulmonary edema .


Adverse Effects-B2 Agonists :10/17/2009 IVMS 43 Adverse Effects-B2 Agonists Excessive cardiovascular stimulation Skeletal muscle tremor (tolerance develops, unknown mechanism) due to ß2 adrenergic receptor activation Overusage may be a factor in morbidity and mortality in asthmatics.


Alpha1 Selective Adrenergic Agonists :10/17/2009 IVMS 44 Alpha1 Selective Adrenergic Agonists Alpha1 selective adrenergic agonists activate a adrenergic receptors in vascular smooth muscle producing vasoconstriction. Peripheral vascular resistance is increased. Blood pressure may be increased, causing a reflex reduction heart rate a1 adrenergic agonists are used clinically in management of hypotension and shock.


Alpha1 Selective Adrenergic Agonists :10/17/2009 IVMS 45 Alpha1 Selective Adrenergic Agonists Direct Acting Phenylephrine (Neo-Synephrine) and methoxamine (Vasoxyl) are direct-acting vasoconstrictors. Mixed Acting Mephentermine (Wyamine) and metaraminol (Aramine) act both by direct receptor activation and by promoting epinephrine release.


Methoxamine (Vasoxyl) :10/17/2009 IVMS 46 Methoxamine (Vasoxyl) specific alpha1 receptor agonist increases peripheral resistance causes an increase in blood pressure that precipitates sinus bradycardia (decreased heart rate) due to vagal reflex. Reflex bradycardia may be block by atropine (muscarinic antagonist) Clinical use: hypotensive states termination (by vagal reflex) of paroxysmal atrial tachycardia (adenosine may be preferable)


Phenylephrine (Neo-Synephrine) :10/17/2009 IVMS 47 Phenylephrine (Neo-Synephrine) Specific alpha1 receptor agonist Increases peripheral resistance Causes an increase in blood pressure that precipitates sinus bradycardia (decreased heart rate) due to vagal reflex. Reflex bradycardia may be block by atropine (muscarinic antagonist) Clinical use: hypotensive states mydriatic nasal decongestant


Alpha 2 Selective Adrenergic Agonists and Miscellaneous Adrenergic Agonists :10/17/2009 IVMS 48 Alpha 2 Selective Adrenergic Agonists and Miscellaneous Adrenergic Agonists alpha2 selective adrenergic agonists are used to treat essential hypertension. Mechanism of action: activation of central a2 adrenergic receptors at cardiovascular control centers activation decreases sympathetic outflow, reducing sympathetic vascular tone.


alpha2 Selective Adrenergic Agonists :10/17/2009 IVMS 49 alpha2 Selective Adrenergic Agonists Clonidine (Catapres) is primarily used in treating essential hypertension. A prolonged hypotensive response results from a decrease in CNS sympathetic outflow. This response is due to a2 selective adrenergic receptor activation


alpha2 Selective Adrenergic Agonists Clonidine (Catapres)(2) :10/17/2009 IVMS 50 alpha2 Selective Adrenergic Agonists Clonidine (Catapres)(2) Adverse Effects: dry mouth sedation sexual dysfuction Clonidine's a2 selective adrenergic receptor activation of vascular smooth muscle may increase blood pressure in patients with severe autonomic dysfunction with profound orthostatic hypotension (in these patients the reduction of central sympathetic outflow in not clinically important)


alpha2 Selective Adrenergic Agonists and Miscellaneous Adrenergic Agonists :10/17/2009 IVMS 51 alpha2 Selective Adrenergic Agonists and Miscellaneous Adrenergic Agonists Alpha-methyl DOPA (methyldopa (Aldomet)), metabolically converted to alpha-methyl norepinephrine, is used for treating essential hypertension A prolonged hypotensive response results from a decrease in CNS sympathetic outflow. This response is due to a2 selective adrenergic receptor activation. Adverse Effects: dry mouth sedation


alpha2 Selective Adrenergic Agonists and Miscellaneous Adrenergic Agonists :10/17/2009 IVMS 52 alpha2 Selective Adrenergic Agonists and Miscellaneous Adrenergic Agonists Amphetamine CNS stimulant (releasing biogenic nerve terminal amines): respiratory center mood elevation decreased perception of fatigue Other effects: headache, palpitations, dysphoria Appetite suppression Weight loss due to decrease food intake psychological tolerance/dependence


Amphetamine (2) Indirect acting sympathomimetic :10/17/2009 IVMS 53 Amphetamine (2) Indirect acting sympathomimetic Toxicity: CNS: restlessness, tremor, irritablity, insomnia, aggressiveness, anxiety, panic, suicidal ideation, etc. Cardiovascular: arrhythmias, hypertension or hypotension, angina GI: dry mouth, anorexia, vomiting, diarrhea, cramping Treatment: urinary acidification by ammonium chloride hypertension: nitroprusside or alpha adrenergic receptor antagonist CNS: sedative-hypnotic drugs


Amphetamine (3) :10/17/2009 IVMS 54 Amphetamine (3) Therapeutic Use: Narcolepsy Obesity Attention-deficit hyperactivity disorder


Methylphenidate (Ritalin) :10/17/2009 IVMS 55 Methylphenidate (Ritalin) Mild CNS stimulant, chemically related to amphetamine Effects more prevalent on mental than motor activities General pharmacological profile similar to amphetamine Major Therapeutic Use: Narcolepsy Attention-deficit hyperactivity disorder


Ephedrine :10/17/2009 IVMS 56 Ephedrine alpha and ß adrenergic receptor agonist Indirect sympathomimetic also, promoting norepinephrine release non-catechol structure, orally active Pharmacological effects: increases heart rate, cardiac output usually increases blood pressure may cause uriniary hesitancy due to stimulation of a smooth muscle receptors in bladder base. bronchodilation: ß adrenergic receptor response


Ephedrine(2) :10/17/2009 IVMS 57 Ephedrine(2) Limited Clinical Use due to better pharmacological alternatives (asthma, heart block, CNS stimulation) Vasoconstrictors for Nasal Mucosal Membranes and for the Eye


Adrenergic Drug Lists Summary :10/17/2009 IVMS 58 Adrenergic Drug Lists Summary Catecholamines


Adrenergic Drug Lists Summary :10/17/2009 IVMS 59 Adrenergic Drug Lists Summary Direct adrenoceptor agonists


Adrenergic Drug Lists Summary :10/17/2009 IVMS 60 Adrenergic Drug Lists Summary Indirect sympathomimetics


Adrenergic Drug Lists Summary :10/17/2009 IVMS 61 Adrenergic Drug Lists Summary Alpha-Adrenoceptor antagonists


Adrenergic Drug Lists Summary :10/17/2009 IVMS 62 Adrenergic Drug Lists Summary ß-Adrenoceptor antagonists


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Adrenergics High Yield Synopsis (1) :10/17/2009 IVMS 64 Adrenergics High Yield Synopsis (1)


Adrenergics High Yield Synopsis(2) :10/17/2009 IVMS 65 Adrenergics High Yield Synopsis(2)


Adrenergics High Yield Synopsis(3) :10/17/2009 IVMS 66 Adrenergics High Yield Synopsis(3)


Adrenergics High Yield Synopsis(4) :10/17/2009 IVMS 67 Adrenergics High Yield Synopsis(4)


Adrenergics High Yield Synopsis(5) :10/17/2009 IVMS 68 Adrenergics High Yield Synopsis(5)