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Pulsatile beta-endorphin release from the human pituitary in vitro
W G Rossmanith1, M Gambacciani, J H Liu
1Department of Reproductive Medicine, School of Medicine, University of California, San Diego, La Jolla 92093.
Summary
Human fetal and adult pituitaries release beta-endorphin in spontaneous, calcium-dependent pulses. This suggests an internal pituitary mechanism controls beta-endorphin release, independent of the hypothalamus.
Area of Science:
- Neuroendocrinology
- Reproductive Biology
- Cellular Physiology
Background:
- The regulation of beta-endorphin release from the anterior pituitary is complex.
- Spontaneous pulsatile release suggests an intrinsic pituitary mechanism may be involved.
Purpose of the Study:
- To characterize spontaneous immunoreactive beta-endorphin (i beta-END) release from human fetal and adult anterior pituitaries in vitro.
- To investigate the role of calcium and corticotropin-releasing factor (CRF) in regulating i beta-END release.
Main Methods:
- In vitro perifusion system used to study anterior pituitaries from human fetuses (20-23 weeks gestation) and adults.
- Calcium channel blockade (verapamil, EGTA) and CRF stimulation were employed.
- Potassium chloride (KCl) was used to assess cellular depolarization.
Main Results:
- Spontaneous i beta-END release was pulsatile in both fetal and adult pituitaries.
- Calcium blockade significantly reduced pulse frequency and amplitude.
- CRF administration induced dose- and time-dependent increases in i beta-END release.
- KCl further enhanced CRF-stimulated release, indicating calcium-dependent exocytosis.
Conclusions:
- Human anterior pituitary i beta-END release is characterized by high-frequency, spontaneous pulses.
- This pulsatile release is calcium-dependent and appears to be regulated by an intrapituitary mechanism, independent of hypothalamic stimulation.
- CRF significantly stimulates i beta-END release in a manner that can be further augmented by direct pituitary cell depolarization.