Evidence that endogenous vasoactive intestinal peptide (VIP) is involved in the regulation of rat pituitary-adrenocortical function: in vivo studies with a VIP antagonist.
Nowak. M M; Markowska. A A; Nussdorfer. G G GG; Tortorella. C C; Malendowicz. L K LK
Key Findings
- A VIP‑blocking peptide (GRF‑1‑29) reduced aldosterone levels in unstressed rats.
- The blocker did not change ACTH or corticosterone (cortisol) levels under baseline conditions.
- During cold stress, the VIP antagonist blunted the normal increase in ACTH, aldosterone, and corticosterone, but it did not affect the response to ether stress.
Practical Outcomes
- The study is done in rats and uses a VIP antagonist, not a supplement people can take. It does not provide any dosage guidance, safety data, or clear benefits for human health, so it offers little actionable information for biohackers or self‑experimenters.
Summary
In rats, a drug that blocks the natural peptide VIP (called GRF‑1‑29) lowered the hormone aldosterone but didn’t change ACTH or cortisol levels under normal conditions. When the rats were stressed by cold, the blocker reduced the usual rise in stress hormones, while it had no effect on stress caused by ether. This suggests VIP helps control aldosterone and is important for the body’s response to cold stress.
Abstract
The effect of a subcutaneous bolus injection of 2 micrograms magnitude of Ac,Tyr1,D-Phe2-GRF(1-29) amide, a specific VIP antagonist (VIP-A), on the hypothalamo-pituitary-adrenocortical (HPA) axis were investigated in both normal and ether- or cold-stressed rats. Blood concentrations of ACTH, aldosterone (ALDO) and corticosterone (B) were measured by specific RIA 1, 2 or 4 h after VIP-A injection. VIP-A administration to normal rats strikingly lowered the plasma concentration of ALDO, without significantly affecting those of ACTH and B. Ether and cold stresses notably raised the blood levels of ACTH, ALDO and B, and these rises lasted unchanged until 4 h. VIP-A did not affect the response of HPA axis to ether stress, but provoked a marked depression of that to cold stress. In light of these findings the following conclusions can be drawn: (i) endogenous VIP does not regulate HPA-axis function under basal conditions, but it plays a pivotal role in the mechanisms involved in the activation of HPA axis induced by cold exposure; and (ii) endogenous VIP exerts a tonic stimulatory action on ALDO secretion, probably by acting directly on the adrenal zona glomerulosa.
Study Information
pubmed
1994
1994-11-01T00:00:00.000Z
10.1016/0143-4179(94)90111-2
13
42