Study summary · research use only
Vasoactive intestinal peptide fragment VIP10-28 and active vasodilation in human skin
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this human study, the authors examined the vasoactive intestinal peptide (VIP) fragment VIP(10-28) as a possible antagonist of VIP-mediated skin vasodilation and active vasodilation (AVD) during heating, across four sub-studies using laser Doppler flowmetry and pharmacologic inhibitors. Contrary to a prior report, they found that VIP(10-28) augmented rather than inhibited vasodilation to exogenous VIP and to hyperthermia (P < 0.05), and that neither nitric oxide synthase inhibition nor an H1 antagonist changed the augmented dilation. They also report that elevated baseline skin blood flow attenuated the percentage rise in cutaneous vascular conductance. The authors conclude VIP(10-28) may be unsuitable as an antagonist for studying VIP-mediated dilation in human skin.
Abstract
A recent study reported the vasoactive intestinal peptide (VIP) fragment VIP(10-28) inhibited the rise in skin blood flow during heat stress. Our laboratory has reported that the nitric oxide (NO) pathway and histamine receptor-1 (H1)-receptor activation is common to both exogenous VIP-mediated dilation and active vasodilation (AVD). The present study aimed to further examine the specific role for VIP in AVD by using VIP(10-28) to antagonize VIP-mediated dilation in the presence of NO synthase (NOS) inhibition and an H1 antagonist. Study 1 (n = 12) examined whether VIP(10-28) antagonizes vasodilation to exogenous VIP via inhibition of NO-dependent mechanisms. Study 2 (n = 6) investigated AVD in skin sites receiving VIP(10-28) alone and in combination with NOS inhibition. Study 3 (n = 6) examined AVD in sites receiving VIP(10-28) alone and combined VIP(10-28) and H1 antagonism. Due to differences in our findings and those previously published, study 4 (n = 6) investigated whether an increase in baseline skin blood flow could result in a diminished rise in AVD. Red blood cell flux was measured using laser Doppler flowmetry, and cutaneous vascular conductance (flux/mean arterial pressure) was normalized to maximal vasodilation (28 mM sodium nitroprusside). VIP(10-28) augmented vasodilation to exogenous VIP (P < 0.05 vs. control) and hyperthermia (P < 0.05 vs. control). NOS inhibition had no effect on the augmented dilation during exogenous VIP or hyperthermia (P > 0.05). Similarly, H1-receptor antagonists had no effect on the augmented dilation during hyperthermia (P > 0.05 vs. VIP(10-28)). In study 4, percentage of maximal cutaneous vascular conductance was attenuated when baseline skin blood flow was elevated before whole body heating. Our results suggest that VIP(10-28) may be an unsuitable antagonist for examining a role for VIP-mediated dilation in human skin.
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