VIP antagonists enhance excitatory cholinergic neurotransmission in the human airway.
Aizawa. H H; Inoue. H H; Shigyo. M M; Takata. S S; Koto. H H; Matsumoto. K K; Hara. N N
Key Findings
- VIP (10⁻¹⁰‑10⁻⁷ M) did not affect airway muscle contractions in human bronchus.
- Two VIP antagonists (10⁻⁸ M) boosted contractions caused by nerve stimulation without changing muscle sensitivity to acetylcholine.
- The results imply that natural VIP normally dampens acetylcholine release from vagus nerves in the human airway, and that external VIP may be quickly broken down.
Practical Outcomes
- For most biohackers, this study offers little direct guidance. It suggests that using VIP‑blocking compounds could increase airway tone, but no safe dosage or protocol is provided. Until more research clarifies benefits and risks, it’s not a practical tool for longevity or performance optimization.
Summary
In human airway tissue, adding the peptide VIP didn't change how the airway muscles contracted, but blocking VIP with specific antagonists made the muscles contract more strongly by increasing the release of acetylcholine, a nerve signal that tightens the airway.
Abstract
It has been reported that a low concentration of exogenously applied vasoactive intestinal peptide (VIP) suppresses the release of acetylcholine (ACh) from vagus nerve terminals in the ferret and feline trachea. There has been, however, no documentation of the prejunctional action of VIP in the human airway. We observed the effects of VIP and VIP antagonists on cholinergic excitatory neuro-effector transmission in the human bronchus to study the possible role of endogenous VIP on excitatory neurotransmission. In the human bronchus, VIP (10(-10) to 10(-7) M) showed no effect on either the contractions evoked by electrical field stimulation (EPS) or those evoked by ACh. To investigate the possible role of endogenous VIP on the human bronchus, we observed the effects of the VIP antagonists [4-Cl-D-Phe6,Leu17]-VIP and [Ac-Tyr1,D-Phe2]-GRF(1-29)-NH2 on excitatory neuro-effector transmission. Both VIP antagonists (10(-8) M) significantly enhances the contractions evoked by EFS without affecting the ACh sensitivity of smooth muscle cells. These results indicate that VIP antagonists have a prejunctional action that enhances excitatory neurotransmission. This study suggests that endogenous VIP may suppresses ACh release from the vagus nerve terminals in the human airway. It is also suggested that exogenously applied VIP may be inactivated by some mechanism in the human airway.
Study Information
pubmed
1994
10.1007/bf00175944