Myogenic and metabolic feedback in cerebral autoregulation: Putative involvement of arachidonic acid-dependent pathways

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Myogenic and metabolic feedback in cerebral autoregulation : Putative involvement of arachidonic acid-dependent pathways. / Berg, Ronan M G.

I: Medical Hypotheses, Bind 92, 07.2016, s. 12-7.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Berg, RMG 2016, 'Myogenic and metabolic feedback in cerebral autoregulation: Putative involvement of arachidonic acid-dependent pathways', Medical Hypotheses, bind 92, s. 12-7. https://doi.org/10.1016/j.mehy.2016.04.024

APA

Berg, R. M. G. (2016). Myogenic and metabolic feedback in cerebral autoregulation: Putative involvement of arachidonic acid-dependent pathways. Medical Hypotheses, 92, 12-7. https://doi.org/10.1016/j.mehy.2016.04.024

Vancouver

Berg RMG. Myogenic and metabolic feedback in cerebral autoregulation: Putative involvement of arachidonic acid-dependent pathways. Medical Hypotheses. 2016 jul.;92:12-7. https://doi.org/10.1016/j.mehy.2016.04.024

Author

Berg, Ronan M G. / Myogenic and metabolic feedback in cerebral autoregulation : Putative involvement of arachidonic acid-dependent pathways. I: Medical Hypotheses. 2016 ; Bind 92. s. 12-7.

Bibtex

@article{a81c2f33aa1e40e6bbe66a91a210467c,
title = "Myogenic and metabolic feedback in cerebral autoregulation: Putative involvement of arachidonic acid-dependent pathways",
abstract = "The present paper presents a mechanistic model of cerebral autoregulation, in which the dual effects of the arachidonic acid metabolites 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) on vascular smooth muscle mediate the cerebrovascular adjustments to a change in cerebral perfusion pressure (CPP). 20-HETE signalling in vascular smooth muscle mediates myogenic feedback to changes in vessel wall stretch, which may be modulated by metabolic feedback through EETs released from astrocytes and endothelial cells in response to changes in brain tissue oxygen tension. The metabolic feedback pathway is much faster than 20-HETE-dependent myogenic feedback, and the former thus initiates the cerebral autoregulatory response, while myogenic feedback comprises a relatively slower mechanism that functions to set the basal cerebrovascular tone. Therefore, assessments of dynamic cerebral autoregulation, which may provide information on the response time of the cerebrovasculature, may specifically be used to yield information on metabolic feedback mechanisms, while data based on assessments of static cerebral autoregulation represent the integrated functionality of myogenic and metabolic feedback. ",
keywords = "Animals, Arachidonic Acid/metabolism, Astrocytes/cytology, Brain/metabolism, Calcium/metabolism, Cerebrovascular Circulation, Endothelial Cells/cytology, Feedback, Physiological, Homeostasis/physiology, Humans, Hydroxyeicosatetraenoic Acids/metabolism, Models, Biological, Models, Theoretical, Muscle Development, Muscle, Smooth, Vascular/metabolism, Oxygen/metabolism, Potassium/metabolism, Signal Transduction",
author = "Berg, {Ronan M G}",
note = "Copyright {\textcopyright} 2016 Elsevier Ltd. All rights reserved.",
year = "2016",
month = jul,
doi = "10.1016/j.mehy.2016.04.024",
language = "English",
volume = "92",
pages = "12--7",
journal = "Medical Hypotheses",
issn = "0306-9877",
publisher = "Churchill Livingstone",

}

RIS

TY - JOUR

T1 - Myogenic and metabolic feedback in cerebral autoregulation

T2 - Putative involvement of arachidonic acid-dependent pathways

AU - Berg, Ronan M G

N1 - Copyright © 2016 Elsevier Ltd. All rights reserved.

PY - 2016/7

Y1 - 2016/7

N2 - The present paper presents a mechanistic model of cerebral autoregulation, in which the dual effects of the arachidonic acid metabolites 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) on vascular smooth muscle mediate the cerebrovascular adjustments to a change in cerebral perfusion pressure (CPP). 20-HETE signalling in vascular smooth muscle mediates myogenic feedback to changes in vessel wall stretch, which may be modulated by metabolic feedback through EETs released from astrocytes and endothelial cells in response to changes in brain tissue oxygen tension. The metabolic feedback pathway is much faster than 20-HETE-dependent myogenic feedback, and the former thus initiates the cerebral autoregulatory response, while myogenic feedback comprises a relatively slower mechanism that functions to set the basal cerebrovascular tone. Therefore, assessments of dynamic cerebral autoregulation, which may provide information on the response time of the cerebrovasculature, may specifically be used to yield information on metabolic feedback mechanisms, while data based on assessments of static cerebral autoregulation represent the integrated functionality of myogenic and metabolic feedback.

AB - The present paper presents a mechanistic model of cerebral autoregulation, in which the dual effects of the arachidonic acid metabolites 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) on vascular smooth muscle mediate the cerebrovascular adjustments to a change in cerebral perfusion pressure (CPP). 20-HETE signalling in vascular smooth muscle mediates myogenic feedback to changes in vessel wall stretch, which may be modulated by metabolic feedback through EETs released from astrocytes and endothelial cells in response to changes in brain tissue oxygen tension. The metabolic feedback pathway is much faster than 20-HETE-dependent myogenic feedback, and the former thus initiates the cerebral autoregulatory response, while myogenic feedback comprises a relatively slower mechanism that functions to set the basal cerebrovascular tone. Therefore, assessments of dynamic cerebral autoregulation, which may provide information on the response time of the cerebrovasculature, may specifically be used to yield information on metabolic feedback mechanisms, while data based on assessments of static cerebral autoregulation represent the integrated functionality of myogenic and metabolic feedback.

KW - Animals

KW - Arachidonic Acid/metabolism

KW - Astrocytes/cytology

KW - Brain/metabolism

KW - Calcium/metabolism

KW - Cerebrovascular Circulation

KW - Endothelial Cells/cytology

KW - Feedback, Physiological

KW - Homeostasis/physiology

KW - Humans

KW - Hydroxyeicosatetraenoic Acids/metabolism

KW - Models, Biological

KW - Models, Theoretical

KW - Muscle Development

KW - Muscle, Smooth, Vascular/metabolism

KW - Oxygen/metabolism

KW - Potassium/metabolism

KW - Signal Transduction

U2 - 10.1016/j.mehy.2016.04.024

DO - 10.1016/j.mehy.2016.04.024

M3 - Journal article

C2 - 27241246

VL - 92

SP - 12

EP - 17

JO - Medical Hypotheses

JF - Medical Hypotheses

SN - 0306-9877

ER -

ID: 236992609