What Are Receptors?

Receptors are
like biological "light switches" which turn on and off when stimulated by a drug
which binds to the receptor and activates it. For example, narcotic pain
relievers like morphine bind to receptors in the brain that sense pain and
decrease the intensity of that perception. Non-narcotic pain relievers like
aspirin, Motrin (ibuprofen) or Tylenol (acetaminophen) bind to an enzyme located
in cells outside of the brain close to where the pain is localized (e.g., hand,
foot, low back, but not in the brain) and decrease the formation of
biologically-active substances known as prostaglandins, which cause pain and
inflammation. These "peripherally-acting" (act outside of the central nervous
system (CNS)) analgesics may also decrease the sensitivity of the local pain
nerves causing fewer pain impulses to be sensed and transmitted to the brain for
appreciation.
In some instances, a drug's site of action or "receptor" may
actually be something which resides within the body, but is not anatomically a
part of the body. For example, when you take an antacid like Tums or Rolaids,
the site of action is the acid in the stomach which is chemically neutralized.
However, if you take an over-the-counter (OTC) medication which inhibits stomach
acid production instead of just neutralizing it (e.g., Tagamet (cimetidine) or
Pepsid-AC (famotidine)), these compounds bind to and inhibit recptors in the
stomach wall responsible for producing acid.
Another example of drugs which
bind to a receptor that is not part of your body are antibiotics. Antibiotics
bind to portions of a bacterium that is living in your body and making you sick.
Most antibiotics inhibit an enzyme inside the bacteria which causes the bacteria
to either stop reproducing or to die from inhibition of a vital biochemical
process.
In many instances, the enzyme in the bacteria does not exist in
humans, or the human form of the enzyme does not bind the inhibiting drug to the
same extent that the bacterial enzyme does, thus providing what pharmacologists
call a "Selective Toxicity". Selective toxicity means that the drug is far more
toxic to the sensitive bacteria than it is to humans thus providing sick
patients with a benefit that far outweighs any risks of direct toxicity. Of
course, this does not mean that certain patients won't be allergic to certain
drugs.
Penicillin is a good example to discuss. Although penicillin inhibits
an enzyme found in sensitive bacteria which helps to "build" part of the cell
wall around the outside of the bacteria, and this enzymatic process does not
occur in human cells, some patients develop an allergy to penicillin (and
related cepahlosporin) antibiotics. This allergy is different from a direct
toxicity and demonstrates that certain people's immune system become
"sensitized" to some foreign drug molecules (xenobiotics) which are not
generally found in the body.
As medical science has learned more about how
drugs act, pharmacologists have discovered that the body is full of different
types of receptors which respond to many different types of drugs. Some
receptors are very selective and specific, while others lack such specificity
and respond to several different types of drug molecules.
To date, receptors
have been identified for the following common drugs, or neurotransmitters* found
in the body: narcotics (morphine), benzodiazepines (Valium, Xanax),
acetylcholine* (nicotinic and muscarinic cholinergic receptors), dopamine*,
serotonin* (5-hydroxytryptamine; 5-HT), epinephrine (adrenalin) and
norepinephrine* (a and b adrenergic receptors), and many
others.
Neurotransmitters* are chemicals released from the end of one neuron
(nerve cell) which diffuse across the space between neurons called the synaptic
cleft and stimulate an adjacent neuron to signal the transmission of
information.
The rest of this section is designed to explain the complicated
journey of a drug through the body, which pharmacologists call
pharmacokinetics.