Analogues of vasoactive intestinal peptide (VIP) contract the guinea-pig uterine artery but do not antagonize VIP-induced relaxations.
Morris. J L JL; Murphy. R R
Key Findings
- Normal guinea‑pig VIP (1‑28) relaxes pre‑contracted uterine artery segments.
- VIP analogues and GRF‑1‑29 do not block VIP‑induced relaxation.
- High concentrations of these analogues (including GRF‑1‑29) produce short‑lived arterial contractions, indicating a second receptor type.
Practical Outcomes
- For biohackers using GRF‑1‑29 or VIP‑based peptides, the data suggest that very high doses might cause temporary blood vessel constriction, which could affect blood pressure or circulation. While the study is in guinea‑pig tissue and not directly translatable to humans, it hints that staying within moderate dosing ranges may avoid potential vascular side effects. No specific dosing protocol or performance benefit is derived from this work.
Summary
The study looked at how different versions of the peptide VIP and a related peptide called GRF‑1‑29 affect blood vessels in guinea‑pig uterine tissue. While normal VIP relaxes the vessels, the tested VIP analogues and GRF‑1‑29 did not block this relaxation but, at very high doses, caused brief vessel tightening. This suggests there are two different receptors for VIP that can have opposite effects on blood vessel tone.
Abstract
Guinea-pig vasoactive intestinal peptide (gpVIP-(1-28] in the concentration range 3 x 10(-9)-3 x 10(-7) mol.1-1 relaxed precontracted segments of the guinea-pig uterine artery. Porcine VIP-(10-28) (pVIP-(10-28], [4-Cl-D-Phe6,Leu17]VIP, or [N-Ac-Tyr1, D-Phe2]GRF-(1-29)-NH2 did not antagonize VIP-induced relaxations of the artery, but high concentrations of the two VIP analogues produced large, transient contractions of the artery. In some preparations 10(-5) mol.1-1 gpVIP-(1-28) also caused transient arterial contractions. These data indicate the presence of two distinct receptors for VIP on the guinea-pig uterine artery, mediating opposite effects on vascular tone.
Study Information
pubmed
1989
1989-03-21T00:00:00.000Z
10.1016/0014-2999(89)90303-8
14
10