Capillary pericytes regulate cerebral blood flow in health and disease

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Capillary pericytes regulate cerebral blood flow in health and disease. / Hall, Catherine N; Reynell, Clare; Gesslein, Bodil; Hamilton, Nicola B; Mishra, Anusha; Sutherland, Brad A; O'Farrell, Fergus M; Buchan, Alastair M; Lauritzen, Martin; Attwell, David.

In: Nature, Vol. 508, No. 7494, 04.2014, p. 55-60.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Hall, CN, Reynell, C, Gesslein, B, Hamilton, NB, Mishra, A, Sutherland, BA, O'Farrell, FM, Buchan, AM, Lauritzen, M & Attwell, D 2014, 'Capillary pericytes regulate cerebral blood flow in health and disease', Nature, vol. 508, no. 7494, pp. 55-60. https://doi.org/10.1038/nature13165

APA

Hall, C. N., Reynell, C., Gesslein, B., Hamilton, N. B., Mishra, A., Sutherland, B. A., O'Farrell, F. M., Buchan, A. M., Lauritzen, M., & Attwell, D. (2014). Capillary pericytes regulate cerebral blood flow in health and disease. Nature, 508(7494), 55-60. https://doi.org/10.1038/nature13165

Vancouver

Hall CN, Reynell C, Gesslein B, Hamilton NB, Mishra A, Sutherland BA et al. Capillary pericytes regulate cerebral blood flow in health and disease. Nature. 2014 Apr;508(7494):55-60. https://doi.org/10.1038/nature13165

Author

Hall, Catherine N ; Reynell, Clare ; Gesslein, Bodil ; Hamilton, Nicola B ; Mishra, Anusha ; Sutherland, Brad A ; O'Farrell, Fergus M ; Buchan, Alastair M ; Lauritzen, Martin ; Attwell, David. / Capillary pericytes regulate cerebral blood flow in health and disease. In: Nature. 2014 ; Vol. 508, No. 7494. pp. 55-60.

Bibtex

@article{868b0541743e4c7bb7617a73ec984507,
title = "Capillary pericytes regulate cerebral blood flow in health and disease",
abstract = "Increases in brain blood flow, evoked by neuronal activity, power neural computation and form the basis of BOLD (blood-oxygen-level-dependent) functional imaging. Whether blood flow is controlled solely by arteriole smooth muscle, or also by capillary pericytes, is controversial. We demonstrate that neuronal activity and the neurotransmitter glutamate evoke the release of messengers that dilate capillaries by actively relaxing pericytes. Dilation is mediated by prostaglandin E2, but requires nitric oxide release to suppress vasoconstricting 20-HETE synthesis. In vivo, when sensory input increases blood flow, capillaries dilate before arterioles and are estimated to produce 84% of the blood flow increase. In pathology, ischaemia evokes capillary constriction by pericytes. We show that this is followed by pericyte death in rigor, which may irreversibly constrict capillaries and damage the blood-brain barrier. Thus, pericytes are major regulators of cerebral blood flow and initiators of functional imaging signals. Prevention of pericyte constriction and death may reduce the long-lasting blood flow decrease that damages neurons after stroke.",
author = "Hall, {Catherine N} and Clare Reynell and Bodil Gesslein and Hamilton, {Nicola B} and Anusha Mishra and Sutherland, {Brad A} and O'Farrell, {Fergus M} and Buchan, {Alastair M} and Martin Lauritzen and David Attwell",
year = "2014",
month = apr,
doi = "10.1038/nature13165",
language = "English",
volume = "508",
pages = "55--60",
journal = "Nature",
issn = "0028-0836",
publisher = "nature publishing group",
number = "7494",

}

RIS

TY - JOUR

T1 - Capillary pericytes regulate cerebral blood flow in health and disease

AU - Hall, Catherine N

AU - Reynell, Clare

AU - Gesslein, Bodil

AU - Hamilton, Nicola B

AU - Mishra, Anusha

AU - Sutherland, Brad A

AU - O'Farrell, Fergus M

AU - Buchan, Alastair M

AU - Lauritzen, Martin

AU - Attwell, David

PY - 2014/4

Y1 - 2014/4

N2 - Increases in brain blood flow, evoked by neuronal activity, power neural computation and form the basis of BOLD (blood-oxygen-level-dependent) functional imaging. Whether blood flow is controlled solely by arteriole smooth muscle, or also by capillary pericytes, is controversial. We demonstrate that neuronal activity and the neurotransmitter glutamate evoke the release of messengers that dilate capillaries by actively relaxing pericytes. Dilation is mediated by prostaglandin E2, but requires nitric oxide release to suppress vasoconstricting 20-HETE synthesis. In vivo, when sensory input increases blood flow, capillaries dilate before arterioles and are estimated to produce 84% of the blood flow increase. In pathology, ischaemia evokes capillary constriction by pericytes. We show that this is followed by pericyte death in rigor, which may irreversibly constrict capillaries and damage the blood-brain barrier. Thus, pericytes are major regulators of cerebral blood flow and initiators of functional imaging signals. Prevention of pericyte constriction and death may reduce the long-lasting blood flow decrease that damages neurons after stroke.

AB - Increases in brain blood flow, evoked by neuronal activity, power neural computation and form the basis of BOLD (blood-oxygen-level-dependent) functional imaging. Whether blood flow is controlled solely by arteriole smooth muscle, or also by capillary pericytes, is controversial. We demonstrate that neuronal activity and the neurotransmitter glutamate evoke the release of messengers that dilate capillaries by actively relaxing pericytes. Dilation is mediated by prostaglandin E2, but requires nitric oxide release to suppress vasoconstricting 20-HETE synthesis. In vivo, when sensory input increases blood flow, capillaries dilate before arterioles and are estimated to produce 84% of the blood flow increase. In pathology, ischaemia evokes capillary constriction by pericytes. We show that this is followed by pericyte death in rigor, which may irreversibly constrict capillaries and damage the blood-brain barrier. Thus, pericytes are major regulators of cerebral blood flow and initiators of functional imaging signals. Prevention of pericyte constriction and death may reduce the long-lasting blood flow decrease that damages neurons after stroke.

U2 - 10.1038/nature13165

DO - 10.1038/nature13165

M3 - Journal article

C2 - 24670647

VL - 508

SP - 55

EP - 60

JO - Nature

JF - Nature

SN - 0028-0836

IS - 7494

ER -

ID: 107903966