Blood oxygen partial pressure affects plasma prolactin concentration in humans

Citation
Hk. Struder et al., Blood oxygen partial pressure affects plasma prolactin concentration in humans, ACT PHYSL S, 165(3), 1999, pp. 265-269
Citations number
18
Categorie Soggetti
Physiology
Journal title
ACTA PHYSIOLOGICA SCANDINAVICA
ISSN journal
00016772 → ACNP
Volume
165
Issue
3
Year of publication
1999
Pages
265 - 269
Database
ISI
SICI code
0001-6772(199903)165:3<265:BOPPAP>2.0.ZU;2-P
Abstract
Responses of plasma prolactin (PRL) concentration to acute and repeated cha nges in blood oxygen partial pressure (Po-2a) at rest were investigated in two studies (A, B), with special reference to possible effects mediated via serotonin (5-HT) synthesis. In A, nine male subjects inhaled for 105 min g as containing different oxygen fractions for 6 days. Gas concentrations con sisted of 14% (A(14)), 21% (A(21))r 40% (A(40)), 60% (A(60)) and 80% (A(80) ) O-2 mixed with Np as well as 100% O-2 (A(100)) Venous and capillary blood samples were drawn before and every 15 min during gas inhalation for analy sis of plasma PRL and Po-2a In B, two groups of subjects (B I; B II) were e xposed to 30 min day(-1) of gas inhalation over 14 consecutive days. Gas co ncentration consisted for B I of 14% O-2/86% N-2 and for B II of 100% O-2 D uring pre- and post-examination a baseline blood sample was drawn, followed by a neuroendocrine test of serotonergic function using a partial 5-HT1A r eceptor agonist (60 mg of buspirone hydrochloride). In A, each increase of inhaled oxygen fraction also resulted in higher blood Po-2a In A(14), A(21) and A(40), plasma PRL concentrations did not change from basal level. Incr eases in plasma PRL concentration were found in A(60) after 30 min as well as in A(80) and A(100) after 15 min. A higher blood Po-2a induced a higher plasma PRL secretion but also an earlier decline from peak plasma PRL value despite continued inhalation of the respective oxygen concentration. Durin g post examination in B, basal plasma PRL concentrations were increased in B I and decreased in B II. Plasma PRL response to stimulation challenge was not affected by treatments. Thus, chronic adaptations of basal plasma PRL concentrations to decreased/increased blood PO2a were not related to up/dow n-regulation, respectively, of central serotonergic receptor function.