Document Detail


Mechanisms of vasoactive intestinal peptide-mediated vasodilation in human skin.
MedLine Citation:
PMID:  15155712     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Vasoactive intestinal peptide (VIP) is known to induce histamine release in human skin and to include a nitric oxide (NO)-dependent dilation in several other vascular beds. However, the relative contribution of histamine and NO to VIP-mediated vasodilation in human skin is unknown. Forty-three subjects volunteered to participate in two studies designed to examine the mechanism of VIP-mediated vasodilation in human skin. Study 1 examined the contribution of NO in the skin blood flow response to eight doses of VIP ranging from 25 to 800 pmol. In addition, study 1 examined a specific role for NO in VIP-mediated dilation. Study 2 examined the relative contribution of NO and histamine to VIP-mediated dilation via H1 and H2 histamine receptors. Infusions were administered to skin sites via intradermal microdialysis. Red blood cell flux was measured by using laser-Doppler flowmetry (LDF), and cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was calculated and normalized to maximal vasodilation. VIP-mediated vasodilation includes a NO-dependent component at doses above 100 pmol, where NO synthase inhibition significantly attenuates CVC (P < 0.05). Inhibition of H1 receptors attenuates the rise in CVC to exogenous VIP (P < 0.05); however, combined H1-receptor inhibition and NO synthase inhibition further reduced VIP-mediated vasodilation compared with either H1 inhibition or NO synthase inhibition alone (P < 0.05). In contrast to H1-receptor inhibition, H2-receptor inhibition did not affect vasodilation to exogenous VIP. Thus, in human skin, VIP-mediated vasodilation includes a NO-dependent component that could not be explained by H1- and H2-receptor activation.
Authors:
Brad W Wilkins; Linda H Chung; Nathan J Tublitz; Brett J Wong; Christopher T Minson
Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, P.H.S.     Date:  2004-05-21
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  97     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-09-10     Completed Date:  2005-04-18     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1291-8     Citation Subset:  IM    
Affiliation:
Department of Human Physiology , University of Oregon, Eugene, Oregon 97403, USA.
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MeSH Terms
Descriptor/Qualifier:
Administration, Topical
Adult
Blood Flow Velocity / drug effects
Dose-Response Relationship, Drug
Female
Humans
Male
Microdialysis / methods
Nitric Oxide / metabolism*
Receptors, Histamine / metabolism*
Skin / blood supply*,  drug effects*
Skin Physiological Phenomena / drug effects*
Vasoactive Intestinal Peptide / administration & dosage*
Vasodilation / drug effects*,  physiology*
Vasodilator Agents / administration & dosage
Grant Support
ID/Acronym/Agency:
R01 HL-70928/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Histamine; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 37221-79-7/Vasoactive Intestinal Peptide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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