ADRENERGIC AGONISTS

 Adrenergic agonists, also called sympathomimetics, are drugs that mimic the effects of the
SNS and are used to stimulate the adrenergic receptors within the SNS. The adverse effects
associated with these drugs are usually also a result of sympathetic stimulation.

 Adrenergic agonists include;

o alpha- and beta-adrenergic agonists
 which stimulate both types of adrenergic receptors in the SNS
o alpha-specific adrenergic agonists
 stimulate only alpha receptors
o beta-specific adrenergic agonists
 stimulate only beta-receptors

 Alpha-specific adrenergic agonists stimulate only the alpha-receptors within the SNS.
Clonidine specifically stimulates alpha2 – receptors and is used to treat hypertension because
its action blocks the release of norepinephrine from nerve axons.

 Many of the beta2 - adrenergic agonists are used to manage and treat asthma, bronchospasm
and other obstructive pulmonary diseases.

 Isoproterenol, a nonspecific beta-specific adrenergic, is used to treat shock, cardiac standstill,

and certain arrhythmias when used systematically; it is especially effective in the treatment f
heart block in transplanted hearts.

 CLASSIFICATION:

 ALPHA-and-BETA ADRENERGIC AGONISTS

 Epinephrine (P)
 Dopamine
 Ephedrine
 Norepinephrine

 ALPHA-SPECIFIC ADRENERGIC AGONISTS

o Alpha-1 specific Adrenergic Agonists:
 Phenylephrine (P)
 Midodrine
o Alpha-2 specific Adrenergic Agonists:
 Clonidine (P)
 Methyldopa

 BETA-SPECIFIC ADRENERGIC AGONISTS : ( Beta1 and Beta2 )

  Isoproterenol (P)
 Albuterol
 Arformoterol
 Indacaterol
 Levalbuterol
 Metaproterenol
 Olodaterol
 Salmeterol
 Terbutaline ?????
o Beta-1 specific adrenergic agonists
 Dobutamine (P)
o Beta-2 specific adrenergic agonists
 Terbutaline
 Isoxsuprine

CHOLINERGIC AGONISTS

 Cholinergic drugs are chemicals that act at the same site as the neurotransmitter ACh,
stimulating the parasympathetic nerves, some nerves in the brain, and the neuromuscular
junction.

 Direct-acting cholinergic drugs react with the ACh receptor sites to cause cholinergic
stimulation.

 Use of direct-acting cholinergic drugs is limited by the systemic effects of the drug. One
drug is used to induce miosis and to treat glaucoma; one agent is available to treat
neurogenic bladder and bladder atony postoperatively or postpartum and another agent is
available to increase GI secretions and relieve the dry mouth of Sjogren’s syndrome.

 All indirect-acting cholinergic drugs are acetylcholinesterase inhibitors. They block

acetylcholinesterase to prevent it from breaking down ACh in the synaptic cleft.

 Cholinergic stimulation by acetylcholinesterase inhibitors is due to an accumulation of

the ACh released from the nerve ending.

 Myasthenia gravis is an autoimmune disease characterized by antibodies to the ACh

receptors. This results in a loss of ACh receptors and eventual loss of resonse at the
neuromuscular junction.

 Acetylcholinesterase inhibitors are used to treat myasthenia gravis because they allow the
accumulation of ACh in the synaptic cleft, prolonging stimulation of any ACh sites that
remain.

 Alzheimer’s disesse is a progressive dementia characterized by a loss of ACh-producing

neurons and ACh receptor sites in the neurocortex.
  Acetylcholineserase inhibitors that corss the blood-brain barrier are used to manage
Alzheimer’s disease by increasing ACh levels in the brain and slowing the progression of
the disease.

 Side effects associated with the use of these drugs are related to stimulation of the
parasympathetic nervous system and may limit the usefulness of some of these drugs.

 CLASSIFICATION:
o DIRECT-ACTING CHOLINERGIC AGONISTS
 Bethanechol (P)
 Carbachol
 Cevimeline
 Pilocarpine

o INDIRECT-ACTING CHOLINERGIC AGONISTS ( AGENTS for

MYASTHENIA GRAVIS )
 Pyridostigmine (P)
 Edrophonium
 Neostigmine

o AGENTS for ALZHEIMER’S DISEASE

 Donepezil (P)
 Galantamine
 Rivastigmine

ADRENERGIC ANTAGONISTS

 Adrenergic blocking agents, or sympatholytic drugs, lyse or block the effects of the SNS

 Both the therapeutic and the adverse effects associated with these drugs are related to their
blocking of the normal responses of the SNS

 The alpha- and beta-adrenergic blocking agents block all of the receptor sites within the SNS,
which results in lower blood pressure, slower pulse and increased renal perfusion with
decreased renin levels. These drugs are indicated for the treatment of essential hypertension.
They are associated with many adverse effects, including the blocking of reflex
bronchodilation, cardiac suppression and diabetic reactions.

 Selective adrenergic blocking agents have been developed that, at therapeutic levels, have
specific affinity for alpha- or beta-receptors for specific alpha1-, beta1- or beta2-receptor sites.
This specificity is lost at levels higher than the therapeutic range.

 Alpha-adrenergic drugs specifically block the alpha receptors of the SNS. At therapeutic
levels, they do not block beta-receptors.
 Nonspecific alpha-adrenergic blocking agents are used to treat pheochromocytoma, a tumor
of the adrenal medulla.

 Alpha1-selective adrenergic blocking agents block the postsynaptic alpha1-receptr sites,

causing a decrease in vascular tone and a vasodilation that leads to a fall in blood pressure
without the reflex tachycardia that occurs when the presynaptic alpha2-receptor sites are also
blocked.

 Beta-blockers are drugs used to block the beta-receptors within the SNS. These drugs are
used for a wide range of conditions, including hypertension, stage fright, migraine, angina
and essential tremors.

 Blockade of all beta-receptors results in a loss of the reflex bronchodilation that occurs with
sympathetic stimulation. This limits the use of these drugs in patients who smoke or have
allergic or seasonal rhinitis, asthma or COPD.

 Beta1-selective adrenergic blocking agents do not block the beta1-receptors that are
responsible for bronchodilation and therefore are preferred in patients with respiratory
problems.

 CLASSIFICATION:
o Nonselective Adrenergic Blocking Agents
 Labetalol (P)
 Amiodarone
 Carvedilol
o Nonselective Alpha-Adrenergic Blocking Agents
 Phentolamine (P)

o Alpha1-Selective Adrenergic Blocking Agents

 Doxaxosin (P)
 Alfuzosin
 Prazosin
 Tamsulosin
 Terazosin
o Nonselective Beta-Adrenergic Blocking Agents
 Propranolol (P)
 Carteolol
 Nadolol
 Sotalol
 Timolol
o Beta1-Selective Adrenergic Blocking Agents
 Atenolol (P)
 Acebutolol
 Betaxolol
 Bisoprolol
 Esmolol
  Metoprolol

CHOLINERGIC ANTAGONISTS
( ANTICHOLINERGIC AGENTS )

 Anticholinergic drugs, also called parasympatholytic drugs, block the effects of ACh at
cholinergic receptor sites, thus blocking the effects of the parasympathetic nervous system.

 Parasympathetic nervous system blockade causes an increase in heart rate, decrease in GI

activity, decrease in urinary bladder tone and function and pupil dilation and cycloplegia.

 These drugs also block cholinergic receptors in the CNS and sympathetic postganglionic
cholinergic receptors, including those that cause sweating.

 Many systemic adverse effects associated with the use of anticholinergic drugs are due to the
systemic cholinergic blocking effects that also produce the desired therapeutic effect.

 Atropine is the most commonly used anticholinergic drug. It is indicated for a wide variety of
conditions and is available in oral, parenteral and topical forms.

 Patients receiving anticholinergic drugs must be monitored for dry mouth, difficulty
swallowing, constipation, urinary retention, tachycardia, pupil dilation and photophobia,
cycloplegia and blurring of vision and heat intolerance caused by a decrease in sweating.

 CLASSIFICATION:
o Anticholinergic Agents / Parasympatholytics
 Atropine (P)
 Dicyclomine
 Fesoterodine
 Glycopyrrolate
 Hyscyamine
 Ipratropium
 Meclizine
 Scopolamine
 Solifenacin
 Toliterodine