Adrenergic Agonists
(Adrenergics or Sympathomimetics)
-Drugs that stimulate the sympathetic nervous system.
-they mimic the sympathetic neurotransmitters norepinephrine and epinephrine
-act on one or more adrenergic receptor sites
adrenergic receptor
-located in the effector cells of muscles, such as the heart, bronchiole walls, gastrointestinal (GI) tract, urinary bladder, and ciliary muscle of the eye
-The four main receptors are alpha1, alpha2, beta1, and beta2
Alpha1
-adrenergic receptor
-located in blood vessels, bladder, eye, prostate
-Increases force of heart contraction; vasoconstriction increases blood pressure; mydriasis (dilation of pupils) occurs; decreases secretion in salivary glands; increases urinary bladd
Alpha2
-adrenergic receptor
-located in postganglionic sympathetic nerve endings
-Inhibits release of norepinephrine; dilates blood vessels; produces hypotension; decreases gastrointestinal motility and tone.
Beta1
-adrenergic receptor
-located in the kidney but primarily in the heart
-Increases heart rate and force of contraction; increases renin secretion, which increases blood pressure.
Beta2
-adrenergic receptor
-located mostly in the smooth muscles of the lung and gastrointestinal tract, the liver, and the uterine muscle.
-Dilates bronchioles; promotes gastrointestinal and uterine relaxation; promotes increase in blood sugar through glycogen
Sympathetic Responses
-Stimulation of the sympathetic nervous system or use of sympathomimetic (adrenergic agonist) drugs can cause...
-pupils and bronchioles to dilate;
-heart rate to increase;
-blood vessels to constrict;
-muscles of the gastrointestinal tract, bladder, and
dopaminergic
-adrenergic receptor
-Only Dopamine can activate this receptor
-located in the renal, mesenteric, coronary, and cerebral arteries
-When this receptor is stimulated, the vessels dilate and blood flow increases.
Transmitters are inactivated by
(1) reuptake of the transmitter back into the neuron (nerve cell terminal)
(2) enzymatic transformation or degradation
(3) diffusion away from the receptor.
Enzymes that inactivate norepinephine
(1) monoamine oxidase (MAO), which is inside the neuron;
(2) catechol-O-methyltransferase (COMT), which is outside of the neuron.
Drugs can prolong the action of the neurotransmitter by...
(1) inhibiting the norepinephrine reuptake, which prolongs the action of the transmitter
(2) inhibiting the degradation of norepinephrine by enzyme action.
sympathomimetic drugs that stimulate adrenergic receptors
-classified into three categories according to their effects on organ cells
-(1) direct-acting sympathomimetics, which directly stimulate the adrenergic receptor (e.g., epinephrine or norepinephrine);
-(2) indirect-acting sympathomimetics, which stimulate
Pseudoephedrine
-mixed-acting sympathomimetic
-acts indirectly by stimulating the release of norepinephrine from the nerve terminals and acts directly on the alpha1 and beta1 receptors
-increases heart rate
-not as potent a vasoconstrictor as epinephrine
-less risk of he
Catecholamines
-the chemical structures of a substance (either endogenous or synthetic) that can produce a sympathomimetic response
endogenous catecholamines examples
-epinephrine
-norepinephrine
-dopamine
synthetic catecholamines examples
-isoproterenol
-dobutamine
Noncatecholamines
-stimulate the adrenergic receptors.
-Most noncatecholamines have a longer duration of action than the endogenous or synthetic catecholamines.
Noncatecholamines examples
-phenylephrine
-metaproterenol
-albuterol
nonselective adrenergic agonists
-stimulate more than one of the adrenergic receptor sites.
-example is epinephrine (Adrenalin), which acts on alpha1-, alpha 2-, beta1-, and beta2-adrenergic receptor sites.
Epinephrine
-trade name: Adrenalin
-Sympathomimetic: adrenergic agonist
-nonselective
-Pregnancy Category: C
-Used for anaphylaxis,asthma, bronchospasm, severe hypotension, cardiac arrest
-increase in blood pressure, pupil dilation, increase in heart rate (tachycardi
Albuterol
-Beta2-adrenergic agonist
-selective
-Trade Names: Proventil, Ventolin
-Pregnancy Category: C
-treats bronchospasm, asthma, bronchitis, and other COPD
-Stimulates beta2-adrenergic receptors in the lungs, which relaxes the bronchial smooth muscle, thus cau
adrenergic blockers (aka adrenergic antagonists, or sympatholytics)
-Drugs that block the effects of adrenergic neurotransmitters by blocking the alpha and beta receptor sites.
-block the effects of the neurotransmitter either
-DIRECTLY by occupying the receptors or
-INDIRECTLY by inhibiting the release of the neurotransm
ALPHA BLOCKERS, Adrenergic blockers effects on alpha1 receptors:
-Vasodilation: decreases blood pressure; reflex tachycardia might result;
-miosis (constriction of pupil) occurs;
-suppresses ejaculation;
-reduces contraction of smooth muscle in bladder neck and prostate gland
BETA BLOCKER, Adrenergic blockers effects on Beta1 receptors:
-Decreases heart rate;
-reduces force of contractions
BETA BLOCKER, Adrenergic blockers effects on Beta2 receptors:
-Constricts bronchioles;
-contracts uterus
-inhibits glycogenolysis, which can decrease blood sugar
ALPHA BLOCKERS
-Drugs that block or inhibit a response at the alpha-adrenergic receptor site
-Selective = block alpha1
-nonselective = block alpha1 and alpha2
-promote vasodilation, causing a decrease in blood pressure
-treat peripheral vascular disease (e.g., Raynaud's
BETA BLOCKERS
-Drugs that block or inhibit a response at the beta adernergic receptor site.
-decrease heart rate, and a decrease in blood pressure usually follows
Atenolol
-Beta1-adrenergic blocker
-Trade Name: Tenormin
-Pregnancy Category: D
-To treat hypertension, angina pectoris, myocardial infarction, and heart failure
-Mode of Action: Selectively blocks beta1-adrenergic receptor sites, decreases sympathetic outflow to
adrenergic neuron blockers
-Drugs that block the release of norepinephrine from the sympathetic terminal neurons
-subdivision of the adrenergic blockers
-used to decrease blood pressure