NOMENCLATURE of Autonomic Drugs

“BLOCKER or ANTAGONIST”: these are used synonymously.

“INHIBITOR”: confined to drugs that inhibit enzymatic pathways, so we speak of anti-

cholinesterase inhibitors for example, which is a specific inhibitor of the cholinesterase enzyme.

MAO INHIBITOR: MonoAmine Oxidase inhibitor

COMT INHIBITOR: Catecholamine O-Methyl Transferase inhibitor

ANTICHOLINESTERASE: another inhibitor of a specific enzyme

CHOLINOMIMETIC: this class of drugs mimics the action of the parasympathetic

nervous system; the drug may not have any structural similarity to acetylcholine, yet mimics the action of this drug.

PARASYMPATHOMIMETIC: synonymous with “cholinomimetic” above; both

mimic the parasympathetic nervous system.

CHOLINERGIC AGONIST: a cholinomimetic drug acts on a cholinergic receptor as

an agonist, this term is used commonly in pharmacology

ANTICHOLINERGIC: Detrol; usually refers to the blocking of the action of the

mediator on its receptor (in the case of detrol, it is blocking the muscarenic receptors to control the patient’s excessive urination). With anticholinergic drugs, always think of the receptor being blocked.

PARASYMPATHOLYTIC: Opposite of parasympathomimetic; parasympathoLYTIC

drugs act as if they’re destroying/modifying/inhibiting the actions of the parasympathetic nervous system… this is an older term and used infrequently nowadays.

MUSCARINIC: this term is difficult to master, comes from an old term for a poisonous

mushroom. This poisonous mushroom contained an alkaloid that acts on a cholinergic receptor—the pharmacologists of yore said that these mushrooms had muscarinic effects, and so these receptors are now labeled M1, M2, M3, M4 and M5.

MUSCARINIC RECEPTOR ANTAGONIST: (ATROPINE) , atropine could also correctly be called an anti-cholinergic

MUSCARINIC RECEPTOR AGONIST: the agonist will stimulate the receptor to

produce a biological response, and is close to a cholinomimetic or parasympathomimetic drug

BELLADONNA ALKALOID: (ATROPINE)… Belladonna translates from Italian as

“beautiful lady”, women would drop this alkaloid plant extract to get mydriasis (pupillary dilation).

SYMPATHOLYTIC: drugs designed to turn off/ inhibit the sympathetic nervous system

(“lytic” means to destroy). The most widely used sympatholytic drugs are the beta blockers.

“BETA-BLOCKER”: shorthand for ‘beta adrenergic receptor blocker’; the suffix

“-olol” distinguishes these drugs

“NON SELECTIVE BETA BLOCKER”: (PROPRANOLOL) there are two beta

adrenergic receptors, beta-1 and beta-2. A non-selective beta blocker will not distinguish between the two.

BETA-ADRENERGIC RECEPTOR ANTAGONIST: (PROPRANOLOL,

ATENOLOL, METOPROLOL, PINDOLOL) dozens of these drugs, the suffix

“-olol” distinguishes these drugs

BETA- 1- ADRENERGIC RECEPTOR BLOCKER: specific beta blocker, see below.

“CARDIOSELECTIVE BETA-BLOCKER”: #1 class of beta blockers prescribed by

cardiologists that block the beta-1 adrenergic receptor relatively selectively. Most beta-1’s are in the myocardium… cardioselective means that it is intended to block the actions of the catecholamines epinephrine and norepinephrine on the cardiac beta-1 receptors and therefore not effect other adrenergic receptors, namely beta-2.

“ALPHA- BLOCKER”: usually prescribed for enlarged prostates—elderly prostates

enlarge and impinge on the prostatic urethra so the old men can’t urinate freely, they don’t have a stream, or they have urgency because they can’t empty their bladder completely because the prostate is impinging on the urethral smooth muscle. It turns out that the bladder area has a lot of sympathetic innervation of smooth muscle, when this is activated it will stimulate the alpha-1 adrenergic receptor causing contraction, when you’ve got contraction you further diminish the patency of the urethra, the pt is unable to urinate. So, the urologist will prescribe an ‘alpha blocker’, the most common is the alpha-1 adrenergic receptor blocker.

ALPHA- 1- ADRENERGIC RECEPTOR BLOCKER: widely used not only in

urology, but also to control HTN because of powerful action on arterial vasculature. Not only affects the prostate, but dilates constricted arteries. So alpha-1 blockers are not only used for prostate enlargement, but HTN. (bonus if the old man has an enlarged prostate and is hypertensive… kill two birds with one stone)

ALPHA-1, BETA-1 BLOCKING AGENT:

SYMPATHOMIMETIC: drugs mimic the action of epinephrine and norepinephrine, for

sympathetic stimulation. Not of the same structural class. Act on adrenergic receptors, alpha-1, alpha-2, beta-1, beta-2.

ADRENERGIC RECEPTOR AGONIST: synonym of sympathomimetic. From the

English term for epinephrine: adrenaline. The term agonist is still valid because it tells you about the physiological response elicited. But be careful! The term can be confusing, later when we talk about analgesics such as codeine, which we use as an analgesic in dentistry (like Tylenol 3, contains acetomenophen plus 30mg codeine), Dr. Levi will ask if codeine is an antagonist—NO! Codeine is an opiate mu receptor agonist. Even though it blocks pain, it does so by acting as an agonist on the opiate receptor, so although the physiologic response may be inhibition, the action is as an agonist. But typically in the autonomic area, when you have an agonist you mimic the effect of sympathetic stimulation.

“BETA-2 BRONCHODILATOR”: most common sympathomimetic/ adrenergic

receptor agonist. Commonly taken by asthmatics. There’s a rich population of beta-2 adrenergic receptors on the bronchial smooth muscle. We can get good bronchodilation by stimulating the beta-2 receptor. Most frequently prescribed bronchodilator, although there are others that also bronchodilators; just because pt has inhaler it isn’t necessarily a beta-2 blocker.

BETA-2- RECEPTOR AGONIST:

BETA-1-RECEPTOR AGONIST:

ALPHA-1-RECEPTOR AGONIST:

ALPHA-2 RECEPTOR AGONIST:

CENTRAL ACTING ALPHA-2 RECEPTOR AGONIST: There are many central

locations in the CNS (particularly in the brainstem and hypothalamus) that are very rich in sympathetic neurons. These have as neurotransmitters norepinephrine or dopamine (catecholamine neurotransmitters). They have, particularly in the blood pressure regulating centers, very rich noradrenergic neurons… we don’t think of them often enough because it turns out that some drugs used for therapeutics are acting centrally on the brain on sympathetic neurons to produce an affect. One of the drugs that I’m thinking of is a central acting alpha-2 receptor agonist. It lowers blood pressure not by acting on the heart or blood vessels or kidney, but by acting centrally on the alpha-2 receptors and turns off the sympathetic outflow to the heart and blood vessels and the blood pressure will drop.

“UPTAKE 1-INHIBITOR”: often referred to in the text as the amine-pump inhibitor,

which is ok by dr. Levi. In the membrane you don’t have a centric pump transporting norepinephrine, but there’s a transporter and an enzyme involved in transporting epinephrine and norepinephrine across the cell membrane. An uptake-1 inhibitor has a significant effect on allowing the accumulation of the neurotransmitter norepinephrine in the synaptic cleft by inhibition of uptake.

“INDIRECT ACTING SYMPATHOMIMETIC”: text doesn’t deal with this well, this

term describes drugs that indirectly act on a cell/ neuron which contains catecholamines, and by indirectly causing a release of the neurotransmitter you get a sympathomimetic effect, as if you had stimulated the adrenergic receptor. They work indirectly, by causing the release of the neurotransmitter. Common one is ephedrine (used in cough meds and at raves—its like injecting a massive dose of adrenaline into your veins).

“GANGLIONIC BLOCKER”: shouldn’t be on national boards or discussed, but he’ll

cover it in case. Blocks both parasympathetic and sympathetic ganglions from transmitting. This isn’t specific at all, but affect both arms of the ANS. Originally used for HTN, but really have no therapeutic value.

“NERUOMUSCULAR BLOCKER”: acetylcholine is a neurotransmitter in skeletal

muscle, must be distinguished from cholinergic responses in smooth muscles. This is distinguished by using the above term. They act specifically on the nicotinic receptor. If acetlycholine is released in saliva and is a transmitter in skeletal muscle, what happens to the pt getting an anti-cholinergic drug? There would be no effect on skeletal muscle function because it’s a nicotinic receptor! So atropine and the classic muscarinic blockers don’t affect neuromuscular transmission in the skeletal muscle. This can be a major conceptual error if you don’t understand the difference between muscarinic and nicotinic receptors.

NICOTINIC GANGLIONIC CHOLINERGIC AGONIST: see above

CATECHOLAMINE: chemical designation for dopamine, epinephrine, norepinephrine

ANTIADRENERGIC: “self-explanatory” interferes with the adrenergic nervous system

Category: Pharmacology Notes