Evidence map›Paper›PMID 28510986›Full record

ArticleMicrocirculation (New York, N.Y. : 1994)2017

Blood pressure normalization via pharmacotherapy improves cutaneous microvascular function through NO-dependent and NO-independent mechanisms.

Daniel H Craighead, Caroline J Smith, Lacy M Alexander

Open access · greenAbstract read
In one paragraph

Article in Microcirculation (New York, N.Y. : 1994), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. AHA/ACC-defined stage 1 hypertensive adults do not display cutaneous microvascular endothelial dysfunction.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Edward F. Adolph Distinguished Lecture: Skin-deep insights into vascular aging.Journal of applied physiology (Bethesda, Md. : 1985) · 2017
    Review
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

3 authors at 2 institutions in 1 country.

Daniel H CraigheadDepartment of Kinesiology, The Pennsylvania State University, University Park, PA, USA.ORCID 0000-0002-8744-5349
Caroline J SmithDepartment of Health & Exercise Science, Appalachian State University, Boone, NC, USA.
Lacy M AlexanderDepartment of Kinesiology, The Pennsylvania State University, University Park, PA, USA.
Pennsylvania State University · USAppalachian State University · US

Funding

Essential Hypertension & Human Skin Blood FlowR01HL093238 · NHLBI · PENNSYLVANIA STATE UNIVERSITY, THE · PI ALEXANDER, LACY M. · 2009 to 2018
$4.3M
Hypercholesterolemia and Human Skin Blood FlowR01HL089302 · NHLBI · PENNSYLVANIA STATE UNIVERSITY, THE · PI KENNEY, W. LARRY · 2007 to 2011
$1.8M
NHLBI NIH HHS R01 HL089302NHLBI NIH HHS R01 HL093238
6 · The paper itself

Abstract

Hypertension is associated with endothelial dysfunction and vascular remodeling.

objectiveTo assess effects of antihypertensive pharmacotherapy on eNOS- and iNOS-dependent mechanisms and maximal vasodilator capacity in the cutaneous microvasculature.

methodsIntradermal microdialysis fibers were placed in 15 normotensive (SBP 111±2 mm Hg), 12 unmedicated hypertensive (SBP 142±2 mm Hg), and 12 medicated hypertensive (SBP 120±2 mm Hg) subjects. Treatments were control, iNOS-inhibited (1400w), and NOS-inhibited (l-NAME). Red cell flux, measured during local heating (42°C) and ACh dose-response protocols, was normalized to CVC (flux MAP

resultsCompared to normotensives, ACh-mediated vasodilation was attenuated in the hypertensive (P<.001), but not in medicated subjects (P=.83). NOS inhibition attenuated ACh-mediated vasodilation in normotensives compared to hypertensive (P<.001) and medicated (P<.001) subjects. With iNOS inhibition, there was no difference in ACh-mediated vasodilation between groups. Compared to the normotensives, local heat-induced vasodilation was attenuated in the hypertensives (P<.001), but iNOS inhibition augmented vasodilation in the hypertensives so this attenuation was abolished (P=.31). Compared to normotensives, maximal vasodilator capacity was reduced in the hypertensive (P=.014) and medicated subjects (P=.004).

conclusionsIn the cutaneous microvasculature, antihypertensive pharmacotherapy improved endothelial function through NO-dependent and NO-independent mechanisms, but did not improve maximal vasodilator capacity.

Indexed as

Antihypertensive AgentsBlood PressureEndothelium, VascularHumansMicrovesselsNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIISkinVasodilationAntihypertensive AgentsNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINOS2 protein, humanNOS3 protein, humancutaneousendotheliumhypertensionmicrovasculaturerenin-angiotensin system

Identifiers

PMID28510986
PMCPMC5672942
OpenAlexW2616676675

What OpenQuestion holds

Textmetadata
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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.