“Whoa! It's like Spotify but for academic articles.”

Instant Access to Thousands of Journals for just $40/month

Get 2 Weeks Free

Vasoactive intestinal peptide fragment VIP10–28 and active vasodilation in human skin

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. histamine receptor-1; cutaneous vascular conductance Address for reprint requests and other correspondence: C. T. Minson, Dept. of Human Physiology, 1240 Univ. of Oregon, Eugene, OR 97403-1240 (e-mail: minson@uoregon.edu ) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

Loading next page...

You're reading a free preview. Subscribe to read the entire article.

And millions more from thousands of peer-reviewed journals, for just $40/month

Get 2 Weeks Free

To be the best researcher, you need access to the best research

  • With DeepDyve, you can stop worrying about how much articles cost, or if it's too much hassle to order — it's all at your fingertips. Your research is important and deserves the top content.
  • Read from thousands of the leading scholarly journals from Springer, Elsevier, Nature, IEEE, Wiley-Blackwell and more.
  • All the latest content is available, no embargo periods.

Stop missing out on the latest updates in your field

  • We’ll send you automatic email updates on the keywords and journals you tell us are most important to you.
  • There is a lot of content out there, so we help you sift through it and stay organized.