VPAC receptor agonist neuropeptide
VIP (vasoactive intestinal peptide)
Neuropeptide activating VPAC1/VPAC2 (Gs-) to relax smooth muscle, modulate secretion, and influence immune tone.
Primary Mechanism of Action
Clinical / Scientific
VIP binds VPAC receptors, raising , relaxing airway and vascular smooth muscle, and modulating T-cell and macrophage profiles in experimental systems. Inhaled VIP analogues have been explored in pulmonary hypertension research.
Pathway Targets
VPAC1/VPAC2
Scientific explanation
Gs- agonism.
Smooth-muscle tone
Scientific explanation
-dependent relaxation.
Pathway Convergence
Clinical / Scientific
Target → pathway → downstream effect → biological consequence. This is a mechanistic map, not a treatment claim.
Receptor to physiology
Target to downstream effect: VPAC1/VPAC2 → Smooth-muscle tone
Mechanistically Relevant Repurposed & Adjunctive Applications
Research peptide context
PreclinicalMechanistic rationale
Catalogued as a research peptide. Mechanistic statements below describe known or pathway biology and do not establish a licensed therapeutic indication.
Mechanistic Application Matrix
| Biological Target | Mechanism | Potential Relevance | Evidence Level |
|---|---|---|---|
| VPAC receptors | Agonism | Vasodilation / immunomodulation | Established mechanism |
In Plain Language
VIP is a gut-and-nerve peptide that raises in its receptors, which can relax muscle in vessels and airways and change immune cell chatter.
Mechanistic information is provided for scientific and educational purposes. Discussion of biological pathways or investigational applications does not establish clinical efficacy or constitute individualized medical advice.