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Published on: December 10, 2014
Blood oxygen partial pressure affects plasma prolactin concentration in humans
H K Strüder1, W Hollmann, H Weicker
1Institute of Sports Games, German Sport University, Cologne.
High blood oxygen levels increase plasma prolactin (PRL) secretion acutely, but chronic exposure leads to adaptive changes in basal PRL levels. Serotonin receptor function was not implicated in these adaptations.
Area of Science:
- Physiology
- Endocrinology
- Neuroscience
Background:
- Plasma prolactin (PRL) regulation is complex and influenced by various physiological factors.
- Oxygen partial pressure (PO2a) is a critical physiological parameter that can affect hormonal responses.
- The role of serotonin (5-HT) in mediating PRL responses to altered oxygen levels requires investigation.
Purpose of the Study:
- To investigate the acute and chronic effects of altered blood oxygen partial pressure on plasma prolactin concentrations.
- To explore potential mediation of these responses via central serotonergic pathways.
Main Methods:
- Two studies (A and B) involving male subjects inhaling different oxygen-nitrogen gas mixtures.
- Study A: Acute exposure (105 min/day for 6 days) to varying oxygen fractions (14%-100%).
- Study B: Chronic exposure (30 min/day for 14 days) to 14% or 100% oxygen, with neuroendocrine testing of serotonergic function using buspirone.
Main Results:
- Acute inhalation of higher oxygen fractions (≥60% O2) increased plasma PRL concentration, with higher PO2a inducing greater secretion.
- Increased PO2a also led to an earlier decline in plasma PRL despite continued oxygen inhalation.
- Chronic exposure to decreased oxygen (14% O2) increased basal PRL, while increased oxygen (100% O2) decreased it; however, PRL response to buspirone was unaffected.
Conclusions:
- Acute hyperoxia stimulates plasma prolactin secretion, but this response is transient.
- Chronic adaptation of basal plasma PRL levels to altered oxygenation occurs independently of central serotonergic receptor function.
- These findings suggest distinct mechanisms for acute PRL regulation by oxygen and long-term adaptation.
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