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Chapter: Clinical Pharmacology: Autonomic nervous system drugs

Adrenergic blocking drugs

Adrenergic blocking drugs, also called sympatholytic drugs, areused to disrupt sympathetic nervous system function.

Adrenergic blocking drugs

Adrenergic blocking drugs, also called sympatholytic drugs, areused to disrupt sympathetic nervous system function. These drugs work by blocking impulse transmission (and thus sympathetic nervous system stimulation) at adrenergic neurons or adrenergic receptor sites. Their action at these sites can be exerted by:


§    interrupting the action of adrenergic (sympathomimetic) drugs


§    reducing available norepinephrine


§    preventing the action of cholinergic drugs.


Classified information


Adrenergic blocking drugs are classified according to their site of action as:


·                 alpha-adrenergic blockers (or alpha blockers)


·                 beta-adrenergic blockers (or beta blockers).


Alpha-adrenergic blockers


Alpha-adrenergic blockers work by interrupting the actions of thecatecholamines epinephrine and norepinephrine at alpha recep-tors. This results in:


·                 relaxation of the smooth muscle in blood vessels


·                 increased dilation of blood vessels


·                 decreased blood pressure.


Drugs in this class include:


·                 alfuzosin


·                 ergoloid mesylates


·                 phenoxybenzamine


·                 phentolamine


·                 prazosin, doxazosin, and terazosin


·                 tamsulosin.


A mixed bag

Ergotamine is a mixed alpha agonist and antagonist; at high doses, it acts as an alpha-adrenergic blocker.




The action of alpha-adrenergic blockers in the body isn’t well un-derstood. Most of these drugs are absorbed erratically when ad-ministered orally, and more rapidly and completely when adminis-tered sublingually. Alpha-adrenergic blockers vary considerably in their onset of action, peak concentration levels, and duration of action.



Alpha-adrenergic blockers work in one of two ways:


·                 They interfere with or block the synthesis, storage, release, and reuptake of norepinephrine by neurons.


·                 They antagonize epinephrine, norepinephrine, or adrenergic (sympathomimetic) drugs at alpha receptor sites.


Not very discriminating


Alpha-adrenergic blockers include drugs that block stimulation of alpha1 receptors and that may block alpha2 receptors.


Reducing resistance

Alpha-adrenergic blockers occupy alpha receptor sites on the smooth muscle of blood vessels. (See How alpha-adrenergicblockers affect peripheral blood vessels.)


This prevents catecholamines from occupying and stimulating the receptor sites. As a result, blood vessels dilate, increasing local blood flow to the skin and other organs. The decreased periph-eral vascular resistance (resistance to blood flow) helps to de-crease blood pressure.


Sympathetic response?


The therapeutic effect of an alpha-adrenergic blocker depends on the sympathetic tone (the state of partial constriction of blood vessels) in the body before the drug is administered. For instance, when the drug is given with the patient lying down, only a small change in blood pressure occurs. In this position, the sympathetic nerves release very little norepinephrine.


Patient up, pressure down


On the other hand, when a patient stands up, norepinephrine is re-leased to constrict the veins and shoot blood back up to the heart. If the patient receives an alpha-adrenergic blocker, however, the veins can’t constrict and blood pools in the legs. Because blood re-turn to the heart is reduced, blood pressure drops. This drop in blood pressure that occurs when a person stands up is called or-thostatic hypotension.




Because alpha-adrenergic blockers cause smooth muscles to relax and blood vessels to dilate, they increase local blood flow to the skin and other organs and reduce blood pressure. As a result, they’re used to treat:


·                 benign prostatic hypertrophy


·                 hypertension


·                 peripheral vascular disorders (diseases of the blood vessels of the extremities), especially those in which blood vessel spasm causes poor local blood flow, such as Raynaud’s disease (intermit-tent pallor, cyanosis, or redness of fingers), acrocyanosis (sym-metrical mottled cyanosis of the hands and feet), and frostbite


·                 pheochromocytoma (a catecholamine-secreting tumor that causes severe hypertension).


Drug interactions


Many drugs interact with alpha-adrenergic blockers, producing a synergistic, or exaggerated, effect. The most serious interactions are severe hypotension and vascular collapse.


These interactions can occur when these drugs are taken with ergoloid mesylates and ergotamine:


·                 Caffeine and macrolide antibiotics can increase the effects of ergotamine.


·                 Dopamine increases the pressor (rising blood pressure) effect.



·                 Nitroglycerin can produce hypotension from excessive dilation of blood vessels.


Sympathomimetics, including many over-the-counter drugs, can increase the stimulating effects on the heart, possibly resulting in hypotension with rebound hypertension. (See Adverse reactionsto alpha-adrenergic blockers.)


Beta-adrenergic blockers


Beta-adrenergic blockers, the most widely used adrenergic block-ers, prevent stimulation of the sympathetic nervous system by in-hibiting the action of catecholamines at beta-adrenergic receptors.


From not so selective…


Beta-adrenergic blockers can be selective or nonselective. Non-selective beta-adrenergic blockers affect:

·                 beta1 receptor sites (located mainly in the heart)

·                 beta2 receptor sites (located in the bronchi, blood vessels, and uterus).


Nonselective beta-adrenergic blockers include carteolol, carvedilol, labetalol, levobunolol, metipranolol, penbutolol, pin-dolol, sotalol, nadolol, propranolol, and timolol. (Carvedilol and labetalol also block alpha1 receptors.)

…to highly discriminating

Selective beta-adrenergic blockers primarily affect beta1-adrenergic sites. They include acebutolol, atenolol, betaxolol, bisoprolol, esmolol, and metoprolol.


The not so beta blockers


Some beta-adrenergic blockers, such as pindolol and acebutolol, have intrinsic sympathetic activity. This means that instead of at-taching to beta receptors and blocking them, these beta-adrenergic blockers attach to beta receptors and stimulate them. These drugs are sometimes classified as partial agonists.




Beta-adrenergic blockers are usually absorbed rapidly and well from the GI tract and are somewhat protein-bound. Food doesn’t inhibit—and may even enhance—their absorption. Some beta-adrenergic blockers are absorbed more completely than others.


Peak by I.V.


The onset of action of beta-adrenergic blockers is primarily dose-and drug-dependent. The time it takes to reach peak concentra-tion levels depends on the administration route. Beta-adrenergic blockers given I.V. reach peak levels much more rapidly than those taken by mouth.




Beta-adrenergic blockers are distributed widely in body tissues, with the highest concentrations found in the:


·                 heart


·                 liver


·                 lungs

·                 saliva.


Metabolism and excretion

Except for nadolol and atenolol, beta-adrenergic blockers are me-tabolized in the liver. They’re excreted primarily in urine, either unchanged or as metabolites, but can also be excreted in feces, bile and, to some degree, breast milk.



Beta-adrenergic blockers have widespread effects in the body be-cause they produce their blocking action not only at adrenergic nerve endings but also in the adrenal medulla.


A matter of the heart


Effects on the heart include increased peripheral vascular resis-tance, decreased blood pressure, decreased force of the heart’s contractions, decreased oxygen consumption by the heart, slowed impulse conduction between the atria and ventricles, and de-creased cardiac output (the amount of blood the heart pumps each minute). (See How beta-adrenergic blockers work.)


Selective and nonselective effects


Some beta-adrenergic blocker effects depend on whether the drug is classified as selective or nonselective.


Selective beta-adrenergic blockers, which prefer to block beta1-receptor sites, reduce stimulation of the heart. They’re often referred to as cardioselective beta-adrenergic blockers.

Nonselective beta-adrenergic blockers, which block both beta1- and beta2-receptor sites, not only reduce stimulation of the heart but also cause the bronchioles of the lungs to constrict. For instance, nonselective beta-adrenergic blockers can cause bron-chospasm in patients with chronic obstructive lung disease. This adverse effect isn’t seen when cardioselective drugs are given at lower doses.




Beta-adrenergic blockers are used to treat many conditions and are under investigation for use in many more. As mentioned previ-ously, their clinical usefulness is based largely (but not exclusive-ly) on how they affect the heart. (See Are beta-adrenergic block-ers underused in elderly patients?)


Helping the heart


Beta-adrenergic blockers can be prescribed after a heart attack to prevent another heart attack or to treat:


·                 angina


·                 heart failure


·                 hypertension


·                 cardiomyopathy (a disease of the heart muscle)


·                 supraventricular arrhythmias (irregular heartbeats that origi-nate in the atria, SA node, or atrioventricular node).


Jack of all trades


Beta-adrenergic blockers are also used to treat:


·                 anxiety


·                 cardiovascular symptoms associated with thyrotoxicosis (over-production of thyroid hormones)


·                 essential tremor


·                 migraine headaches


·                 open-angle glaucoma


·                 pheochromocytoma (tumor of the adrenal gland).


Drug interactions


Many drugs can interact with beta-adrenergic blockers to cause potentially dangerous effects. Some of the most serious effects in-clude cardiac or respiratory depression, arrhythmias, severe bronchospasm, and severe hypotension that can lead to vascular collapse. Other interactions can also occur:


·                 Increased effects or toxicity can occur when cimetidine, digox-in, or calcium channel blockers (primarily verapamil) are taken with beta-adrenergic blockers.


·                 Decreased effects can occur when rifampin, antacids, calcium salts, barbiturates, or anti-inflammatories, such as indomethacin and salicylates, are taken with beta-adrenergic blockers.


·                 Lidocaine toxicity may occur when lidocaine is taken with beta-adrenergic blockers.


·                 The requirements for insulin and oral antidiabetic drugs can be altered when these drugs are taken with beta-adrenergic blockers.


·                 The ability of theophylline to produce bronchodilation is im-paired by nonselective beta-adrenergic blockers.


·                 Clonidine taken with a nonselective beta-adrenergic blocker can cause life-threatening hypertension during clonidine withdrawal.


·                 Sympathomimetics taken with nonselective beta-adrenergic blockers can cause hypertension and reflex bradycardia. (See Ad-verse reactions to beta-adrenergic blockers.)



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