Plasma beta-endorphin and beta-lipotropin in patients with Parkinson's disease.
Experimental and human data in young volunteers suggest that tuberoinfundibular dopaminergic systems physiologically inhibit pituitary secretion of beta-endorphin. This hypothesis was verified in patients with Parkinson's disease, a human model of a selective deficit of dopamine. Both previously untreated patients and patients who had been without chronic treatment for 1 week showed plasma beta-endorphin levels significantly higher than those of healthy age-matched controls. Plasma beta-lipotropin levels of patients and of controls were similar. There was no correlation between plasma opioid levels and age, severity, or duration of the disease. In five patients retested during chronic treatment, plasma levels both of beta-endorphin and of beta-lipotropin significantly decreased. This decrease approximately paralleled clinical improvement. The finding that in Parkinson's disease there is a reversible disinhibition of pituitary secretion of beta-endorphin confirms that this secretion is physiologically inhibited by tuberoinfundibular dopaminergic systems.
D000368:Aged; D004298:Dopamine / Q000502:physiology; D004723:Endorphins / Q000097:blood* / Q000378:metabolism; D005260:Female; D006801:Humans; D007031:Hypothalamus / Q000503:physiopathology; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D010902:Pituitary Gland / Q000378:metabolism; D001615:beta-Endorphin; D008083:beta-Lipotropin / Q000097:blood*
D004723:Endorphins; D007980:Levodopa; D001615:beta-Endorphin; D008083:beta-Lipotropin; D004298:Dopamine