Growth hormone and prolactin stimulation by Madopar in Parkinson's disease

Publisher Website
Google Scholar
Abstract
Madopar, a combination of L-dopa with benserazide, induced an inconsistent rise in plasma growth hormone in unmedicated patients with Parkinson''s disease and in controls, and a greater growth hormone rise in Parkinsonian subjects on chronic Madopar therapy. In subjects on chronic therapy with L-dopa and carbidopa (Sinemet), the growth hormone releasing effect of Madopar was blunted. Madopar increased plasma prolactin (PRL) in controls, unmedicated patients and patients on Madopar therapy while in patients on Sinemet therapy the PRL-releasing effect of Madopar was strikingly reduced. Since these data were interpreted as due to a defective dopamine tone in the hypothalamus of Parkinsonian subjects on Madopar but not Sinemet therapy, a direct dopamine receptor agonist, lisuride, was administered. Lisuride elicited a blunted growth hormone response both in patients on Madopar and Sinemet therapy, without revealing a state of supersensitivity of dopamine receptors for growth hormone control in Parkinsonian subjects on Madopar therapy. No difference was present in the PRL-lowering effect of lisuride in the different experimental groups. Evidently, hypothalamic dopamine function is impaired in Parkinsonian subjects on Madopar therapy, preserved in unmedicated patients, and enhanced in patients on Sinemet therapy. The endocrine effects observed in Parkinsonian subjects on chronic Madopar therapy may be due to some penetration of benserazide across the blood-brain barrier in the region of the hypothalamus. Since Madopar and Sinemet are in essence equally effective antiparkinsonian remedies, penetration of benserazide probably does not occur across the blood-brain barrier surrounding the nigrostriatal system.