Evidence map›Paper›PMID 26368324›Full record

ArticleJournal of vascular research2015

Integration and Modulation of Intercellular Signaling Underlying Blood Flow Control.

Steven S Segal

Abstract read
In one paragraph

Article in Journal of vascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
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  8. Article
  9. Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems.American journal of physiology. Heart and circulatory physiology · 2023
    Review
  10. Review
  11. Endothelial Connexins in Developmental and Pathological Angiogenesis.Cold Spring Harbor perspectives in medicine · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Optical coherence tomography of arteriolar diameter and capillary perfusion during spreading depolarizations.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  19. Review: Circadian clocks and rhythms in the vascular tree.Current opinion in pharmacology · 2021
    Review
  20. ATP and acetylcholine interact to modulate vascular tone and αJournal of applied physiology (Bethesda, Md. : 1985) · 2021
    Article
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

1 author.

Steven S Segal

Funding

Intercellular Coordination of Blood Flow ControlR37HL041026 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SEGAL, STEVEN S · 2008 to 2018
$3.7M
Microcirculation in Aging Skeletal MuscleR01HL086483 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SEGAL, STEVEN S · 2007 to 2012
$2.4M
UNIT CONTROL OF MUSCLE BLOOD FLOWR01HL056786 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SEGAL, STEVEN S · 1996 to 2007
$1.6M
NHLBI NIH HHS R01 HL056786NHLBI NIH HHS R01-HL056786NHLBI NIH HHS R01 HL086483NHLBI NIH HHS R01-HL086483NHLBI NIH HHS R37 HL041026NHLBI NIH HHS R37-HL041026
6 · The paper itself

Abstract

Vascular resistance networks control tissue blood flow in concert with regulating arterial perfusion pressure. In response to increased metabolic demand, vasodilation arising in arteriolar networks ascends to encompass proximal feed arteries. By reducing resistance upstream, ascending vasodilation (AVD) increases blood flow into the microcirculation. Once initiated, e.g. through local activation of K(+) channels in endothelial cells (ECs), hyperpolarization is conducted through gap junctions along the endothelium. Via EC projections through the internal elastic lamina, hyperpolarization spreads into the surrounding smooth-muscle cells (SMCs) through myoendothelial gap junctions (MEGJs) to promote their relaxation. Intercellular signaling through electrical signal transmission (i.e. cell-to-cell conduction) can thereby coordinate vasodilation along and among the branches of microvascular resistance networks. Perivascular sympathetic nerve fibers course through the adventitia and release norepinephrine to stimulate SMCs via α-adrenoreceptors to produce contraction. In turn, SMCs can signal ECs through MEGJs to activate K(+) channels and attenuate sympathetic vasoconstriction. Activation of K(+) channels along the endothelium will dissipate electrical signal transmission and inhibit AVD, thereby restricting blood flow into the microcirculation while maintaining peripheral resistance and perfusion pressure. This review explores the origins and nature of the intercellular signaling that governs blood flow control in skeletal muscle with respect to the interplay between AVD and sympathetic innervation. Whereas these interactions are integral to daily activity and athletic performance, determining the interplay between respective signaling events provides insight into how selective interventions can improve tissue perfusion and oxygen delivery during vascular disease.

Indexed as

HemodynamicsMechanotransduction, CellularMicrocirculationAnimalsAwards and PrizesBlood Flow VelocityCell CommunicationEndothelium, VascularHumansMicrovesselsMuscle ContractionMuscle, SkeletalMuscle, Smooth, VascularRegional Blood FlowSympathetic Nervous SystemVascular Diseases

Identifiers

PMID26368324
PMCPMC4670584

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Registered trials

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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.