In human skin, VIP-mediated vasodilation includes a NO-dependent component at doses above 100 pmol, where NO synthase inhibition significantly attenuated cutaneous vascular conductance.
In plain wordsIn human skin, VIP-induced vessel widening partly depends on nitric oxide at doses above 100 pmol.
- Outcome
- DecreaseNitric oxide contribution to VIP-mediated vasodilation
- Study
n: not reported in source
- Comparator
- Without NO synthase inhibition
- Outcome group
- Vascular function · Cardiovascular
- Studied dose
- 25-800 pmol · intradermal microdialysisAs given in this study (human).
Measurements
- Dose threshold for NO-dependent component
- > 100 pmol
- VIP
Source sentences
VIP-mediated vasodilation includes a NO-dependent component at doses above 100 pmol, where NO synthase inhibition significantly attenuates CVC (P < 0.05).
3 context sentences(design, population, supporting numbers)
Study 1 examined the contribution of NO in the skin blood flow response to eight doses of VIP ranging from 25 to 800 pmol.
Forty-three subjects volunteered to participate in two studies designed to examine the mechanism of VIP-mediated vasodilation in human skin.
Infusions were administered to skin sites via intradermal microdialysis.