[Prostaglandin D2-endogenous regulator of physiological sleep-inhibited CRF-induced ACTH secretion from rat anterior pituitary cells].
Kudo. M M; Kudo. T T; Matsuki. A A
Key Findings
- PGD2 (2 nM) significantly reduced CRF‑induced ACTH release from rat pituitary cells.
- PGE2 (2 nM) also inhibited CRF‑induced ACTH release, with a slightly stronger effect than PGD2.
- Neither PGD2 nor PGE2 affected basal (unstimulated) ACTH levels at the tested concentrations.
Practical Outcomes
- The study shows that PGD2 can dampen stress‑hormone release at the pituitary level in rats, but it does not provide any dosage, safety, or efficacy data for humans. For biohackers, this means the finding is interesting for understanding sleep‑stress links, yet it offers no direct protocol or supplement recommendation to try.
Summary
In a lab study with rat pituitary cells, researchers found that a sleep‑related molecule called prostaglandin D2 (PGD2) can block the hormone‑releasing signal (CRF) that normally makes the pituitary release ACTH, a stress‑related hormone. The effect was seen at very low concentrations and was similar to another sleep factor, DSIP.
Abstract
Delta sleep-inducing peptide (DSIP) is described as being an endogenous sleep factor. This DSIP inhibits ACTH release induced by CRF from rat anterior pituitary tissue. Prostaglandin D2 (PGD2) is regarded as another endogenous sleep factor. However, little information has been accumulated concerning the involvement of PGD2 in the regulation of hormone secretion from the anterior pituitary. It was, therefore, interesting to observe the effect of PGD2 on ACTH release from rat anterior pituitary cells. Rat anterior pituitary cells were obtained by enzymatic digestion of the pituitary gland of male Wister rats. The cell pellet was suspended in Hank's balanced salt solution containing 0.1% BSA and distributed in a 800 microliter aliquot to 12 x 75mm glass tubes. The samples were preincubated for 90 min. in a 37 degrees C waterbath under 5% CO2/95% O2. After preincubation, aliquots of various concentrations of CRF, PGD2 and PGE2 were added in a 100 microliter volume and incubated for 4 hr. ACTH in the incubation medium was determined by radioimmunoassay. 0.01-1.0nM CRF significantly increased the ACTH release from rat anterior pituitary cells in a dose dependent manner. Each concentration of 0.1, 1, 2nM PGD2 or PGE2 had no effect on basal ACTH levels. 2nM PGD2 showed a significant inhibition of the CRF-induced ACTH secretion from rat anterior pituitary cells. Similarly, 2nM PGE2 significantly inhibited the CRF-induced ACTH release from rat anterior pituitary cells. The magnitude of the inhibitory effect of PGE2 was slightly higher than that of PGD2. From these results, we concluded that PGD2 inhibited CRF-induced ACTH secretion at the level of pituitary gland.(ABSTRACT TRUNCATED AT 250 WORDS)
Study Information
pubmed
1990
1990-11-20T00:00:00.000Z
10.1507/endocrine1927.66.11_1158