There is a widespread distribution of dopamine receptors throughout the body (1). From the viewpoint of the treatment of Parkinson's disease, these can be divided into three main anatomical divisions: (a) inside the brain; (b) inside the brain, but outside the blood-brain barrier for dopamine, decarboxylase inhibitors, and domperidone. This group probably includes dopamine receptors in the chemotrigger receptor zone in the area postrema within the fourth ventricle, and possibly hypothalamic dopamine systems involved in endocrine control; (c) peripheral dopamine receptors.
The pituitary dopamine (D2) receptor and vascular dopamine receptors have been known for some time (2–5). Dopamine receptors have been characterized in the animal stomach (6), the retina (7), the carotid body (8,9), and the superior cervical ganglion (10).
There are substantial differences between dopamine receptors in the brain and those in peripheral tissues (11). Major behavioural effects of levodopa that are usually attributed at least in part to peripheral dopamine receptor stimulation, or at least to stimulation of brain receptors outside the blood-brain barrier, and that can be prevented by either decarboxylase inhibitors or domperidone, include (a) nausea and vomiting (stimulation of area postrema and gastric dopamine receptors); (b) hypotension (stimulation of renal and mesenteric vascular receptors); (c) hypoprolactinaemia (stimulation of pituitary receptors); and (d) alteration in respiratory control mechanisms (stimulation of carotid body receptors). In addition, in both normal and parkinsonian subjects, but not in acromegalics, levodopa causes stimulation of pituitary growth hormone release, probably by stimulation of hypothalamic dopamine systems.
© Williams & Wilkins 1986. All Rights Reserved.