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The following explains the function of dopamine agonists in treating PD.  It
is from the European Parkinson's Disease Association.

Peggy


Dopamine receptor agonists (DAs) are drugs that have a structure very
similar to dopamine. Because of this similarity, they are able to mimic the
action of dopamine rather than replenish the inadequate supply of dopamine
in the way levodopa does. If one imagines dopamine as being a key (agonist)
which only fits a specific lock (receptor) to let a door open (body
movement), losing the key to the door means that the door cannot be opened.
Thus, the loss of dopamine means that the receptors will not receive the
signal telling the body to move properly. But because DAs have a similar
structure to dopamine, they are able to fit into the dopamine receptor,
therefore resulting in the same signal being sent that occurs with dopamine
in the non-diseased state. This means that as long as DAs are being taken,
normal control of body movement is restored.

There are several types of receptors for dopamine in the striatum, the D1
and D2 receptors being the most investigated. Similarly there are many
different kinds of DAs, the difference lying in the amount of activity that
they have for a specific dopamine receptor subtype. While some DAs are
unselective and stimulate both D1 and D2 receptors (pergolide), others, such
as bromocriptine and the most recently developed DAs, ropinirole and
pramipexole, selectively stimulate the D2 receptor but not the D1 subtype.
These variations affect not only how well they work in controlling the
symptoms of PD, but also account for the difference in side effects that a
patient may experience on one particular drug compared to another.
The main side-effects of DAs are nausea, vomiting, and a lowering of blood
pressure caused by changes in posture (orthostatic hypotension). These are
usually caused by the action of DAs at dopamine receptors found in other
areas of the brain or body that are not involved in movement or PD. To avoid
such side-effects, the dose of DAs taken is usually increased slowly by the
primary care physician until the appropriate dose is reached, signalled by
the improvement of motor symptoms and hopefully without the emergence of
side-effects. Alternatively, a drug such as domperidone, which prevents the
stimulation of D2 receptors outside the brain, may be prescribed to treat
unwanted side effects from DAs. Other, more severe side-effects may include
hallucinations and psychotic reactions. These can often be minimized by
decreasing the dose of the DA or by taking drugs such as clozapine.
Compared to levodopa, DAs have a slightly longer duration of action and may
suit some people better than levodopa. DAs can be taken as initial therapy
for newly diagnosed patients. In patients at a later stage of disease, whose
response to levodopa therapy is no longer predictable, DAs can be given
together with levodopa to 'smooth out' the control of symptoms. Your doctor
must carefully weight the pros and cons of the different treatments
available and tailor your therapy according to your needs in order to
provide you with the best PD symptom control possible without causing
disturbing side effects.
Source:  http://www.epda.eu.com/medInfo/medInfo-DopamineAgonists.shtm

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