Evidence map›Paper›PMID 20395540›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2010

VIP/PACAP receptor mediation of cutaneous active vasodilation during heat stress in humans.

Dean L Kellogg, Joan L Zhao, Yubo Wu, John M Johnson

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  12. Intradermal administration of ATP augments methacholine-induced cutaneous vasodilation but not sweating in young males and females.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Dean L KelloggDivision of Geriatrics and Gerontology, Department of Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229, USA. kelloggd@uthscsa.edu
Joan L Zhao
Yubo Wu
John M Johnson
South Texas Veterans Health Care System · USNational Center for Geriatrics and Gerontology · JPThe University of Texas Health Science Center at San Antonio · US

Funding

MECHANISMS OF CUTANEOUS ACTIVE VASODILATIONR01HL065599 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KELLOGG, DEAN L · 2000 to 2008
$2.0M
NHLBI NIH HHS HL-065599NHLBI NIH HHS R01 HL065599
6 · The paper itself

Abstract

Vasoactive intestinal peptide (VIP) is implicated in cutaneous active vasodilation in humans. VIP and the closely related pituitary adenylate cyclase activating peptide (PACAP) act through several receptor types: VIP through VPAC1 and VPAC2 receptors and PACAP through VPAC1, VPAC2, and PAC1 receptors. We examined participation of VPAC2 and/or PAC1 receptors in cutaneous vasodilation during heat stress by testing the effects of their specific blockade with PACAP6-38. PACAP6-38 dissolved in Ringer's was administered by intradermal microdialysis at one forearm site while a control site received Ringer's solution. Skin blood flow was monitored by laser-Doppler flowmetry (LDF). Blood pressure was monitored noninvasively and cutaneous vascular conductance (CVC) calculated. A 5- to 10-min baseline period was followed by approximately 70 min of PACAP6-38 (100 microM) perfusion at one site in normothermia and a 3-min period of body cooling. Whole body heating was then performed to engage cutaneous active vasodilation and was maintained until CVC had plateaued at an elevated level at all sites for 5-10 min. Finally, 58 mM sodium nitroprusside was perfused through both microdialysis sites to effect maximal vasodilation. No CVC differences were found between control and PACAP6-38-treated sites during normothermia (19 +/- 3%max untreated vs. 20 +/- 3%max, PACAP6-38 treated; P > 0.05 between sites) or cold stress (11 +/- 2%max untreated vs. 10 +/- 2%max, PACAP6-38 treated, P > 0.05 between sites). PACAP6-38 attenuated the increase in CVC during whole body heating when compared with untreated sites (59 +/- 3%max untreated vs. 46 +/- 3%max, PACAP6-38 treated, P < 0.05). We conclude that VPAC2 and/or PAC1 receptor activation is involved in cutaneous active vasodilation in humans.

Indexed as

AdultBody Temperature RegulationFemaleForearmHeat-Shock ResponseHot TemperatureHumansMaleNitroprussidePituitary Adenylate Cyclase-Activating PolypeptideReceptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type IReceptors, Vasoactive Intestinal Peptide, Type IISkinVasoactive Intestinal PeptideVasodilationVasodilator AgentsNitroprussidePituitary Adenylate Cyclase-Activating PolypeptideReceptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type IReceptors, Vasoactive Intestinal Peptide, Type IIVasoactive Intestinal PeptideVasodilator Agents

Identifiers

PMID20395540
PMCPMC2904198
OpenAlexW2088699050

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.