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Gastrin responses in patients with adrenergic insufficiency
R J Polinsky1, I L Taylor, V Weise
1Clinical Neuropharmacology Section, N.I.N.C.D.S., Bethesda, MD 20892.
Journal of Neurology, Neurosurgery, and Psychiatry
|January 1, 1988
Summary
High gastrin levels in autonomic failure may stem from vagus nerve issues or adrenergic supersensitivity. Multiple system atrophy shows reduced gastrin release due to central sympathetic nervous system deficits.
Area of Science:
- Neuroendocrinology
- Autonomic Nervous System Physiology
Background:
- Autonomic failure involves disruptions in the autonomic nervous system.
- Gastrin regulation is complex and influenced by neural pathways.
Purpose of the Study:
- To investigate gastrin level regulation in autonomic failure.
- To differentiate mechanisms in pure autonomic failure versus multiple system atrophy.
Main Methods:
- Assessed basal and hypoglycemia-induced gastrin levels.
- Studied patients with pure autonomic failure and multiple system atrophy.
Main Results:
- Pure autonomic failure showed high basal gastrin, potentially due to vagus nerve involvement and adrenergic supersensitivity.
- Multiple system atrophy exhibited a reduced gastrin increment post-hypoglycemia, indicating diminished central sympathetic activation.
Conclusions:
- Peripheral vagus nerve and adrenergic supersensitivity may explain high gastrin in pure autonomic failure.
- Reduced central sympathetic activity, not peripheral supersensitivity, underlies altered gastrin release in multiple system atrophy.