Andreas Roepstorff

Dietary nitrate facilitates an acetazolamide-induced increase in cerebral blood flow during visual stimulation

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Dietary nitrate facilitates an acetazolamide-induced increase in cerebral blood flow during visual stimulation. / Aamand, Rasmus; Ho, Yi-Ching Lynn; Dalsgaard, Thomas; Roepstorff, Andreas; Lund, Torben Ellegaard.

In: Journal of Applied Physiology, 01.02.2014.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

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@article{4079eb84291f4e5c81bbe75eedb40449,
title = "Dietary nitrate facilitates an acetazolamide-induced increase in cerebral blood flow during visual stimulation",
abstract = "The carbonic anhydrase (CA) inhibitor acetazolamide (AZ) is used routinely to estimate cerebrovascular reserve capacity in patients, as it reliably increases cerebral blood flow (CBF). However, the mechanism by which AZ accomplishes this CBF increase is not entirely understood. We recently discovered that CA can produce nitric oxide (NO) from nitrite and that AZ enhances this NO production in vitro. In fact, this interaction between AZ and CA accounted for a large part of AZ's vasodilatory action, which fits well with the known vasodilatory potency of NO. The present study aimed to assess whether AZ acts similarly in vivo in the human cerebrovascular system. Hence, we increased or minimized the dietary intake of nitrate in 20 healthy male participants, showed them a full-field flickering dartboard and measured their CBF response to this visual stimulus with arterial spin labeling. Doing so, we found a significant positive interaction between the dietary intake of nitrate and the CBF modulation afforded by AZ during visual stimulation. In addition, but contrary to studies conducted in elderly participants, we report no effect of nitrate intake on resting CBF in healthy human participants. The present study provides in vivo support for an enhancing effect of AZ on the NO production from nitrite catalyzed by CA in the cerebrovascular system. Furthermore our results, in combination with the results of other groups, indicate that nitrate may have significant importance to vascular function when the cerebrovascular system is challenged by age or disease.",
author = "Rasmus Aamand and Ho, {Yi-Ching Lynn} and Thomas Dalsgaard and Andreas Roepstorff and Lund, {Torben Ellegaard}",
year = "2014",
month = feb,
day = "1",
doi = "10.1152/japplphysiol.00797.2013",
language = "English",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "AMER PHYSIOLOGICAL SOC",

}

RIS

TY - JOUR

T1 - Dietary nitrate facilitates an acetazolamide-induced increase in cerebral blood flow during visual stimulation

AU - Aamand, Rasmus

AU - Ho, Yi-Ching Lynn

AU - Dalsgaard, Thomas

AU - Roepstorff, Andreas

AU - Lund, Torben Ellegaard

PY - 2014/2/1

Y1 - 2014/2/1

N2 - The carbonic anhydrase (CA) inhibitor acetazolamide (AZ) is used routinely to estimate cerebrovascular reserve capacity in patients, as it reliably increases cerebral blood flow (CBF). However, the mechanism by which AZ accomplishes this CBF increase is not entirely understood. We recently discovered that CA can produce nitric oxide (NO) from nitrite and that AZ enhances this NO production in vitro. In fact, this interaction between AZ and CA accounted for a large part of AZ's vasodilatory action, which fits well with the known vasodilatory potency of NO. The present study aimed to assess whether AZ acts similarly in vivo in the human cerebrovascular system. Hence, we increased or minimized the dietary intake of nitrate in 20 healthy male participants, showed them a full-field flickering dartboard and measured their CBF response to this visual stimulus with arterial spin labeling. Doing so, we found a significant positive interaction between the dietary intake of nitrate and the CBF modulation afforded by AZ during visual stimulation. In addition, but contrary to studies conducted in elderly participants, we report no effect of nitrate intake on resting CBF in healthy human participants. The present study provides in vivo support for an enhancing effect of AZ on the NO production from nitrite catalyzed by CA in the cerebrovascular system. Furthermore our results, in combination with the results of other groups, indicate that nitrate may have significant importance to vascular function when the cerebrovascular system is challenged by age or disease.

AB - The carbonic anhydrase (CA) inhibitor acetazolamide (AZ) is used routinely to estimate cerebrovascular reserve capacity in patients, as it reliably increases cerebral blood flow (CBF). However, the mechanism by which AZ accomplishes this CBF increase is not entirely understood. We recently discovered that CA can produce nitric oxide (NO) from nitrite and that AZ enhances this NO production in vitro. In fact, this interaction between AZ and CA accounted for a large part of AZ's vasodilatory action, which fits well with the known vasodilatory potency of NO. The present study aimed to assess whether AZ acts similarly in vivo in the human cerebrovascular system. Hence, we increased or minimized the dietary intake of nitrate in 20 healthy male participants, showed them a full-field flickering dartboard and measured their CBF response to this visual stimulus with arterial spin labeling. Doing so, we found a significant positive interaction between the dietary intake of nitrate and the CBF modulation afforded by AZ during visual stimulation. In addition, but contrary to studies conducted in elderly participants, we report no effect of nitrate intake on resting CBF in healthy human participants. The present study provides in vivo support for an enhancing effect of AZ on the NO production from nitrite catalyzed by CA in the cerebrovascular system. Furthermore our results, in combination with the results of other groups, indicate that nitrate may have significant importance to vascular function when the cerebrovascular system is challenged by age or disease.

U2 - 10.1152/japplphysiol.00797.2013

DO - 10.1152/japplphysiol.00797.2013

M3 - Journal article

C2 - 24336884

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

ER -