Neuronal NO promotes cerebral cortical hyperemia during cortical spreading depression in rabbits

Neuronal NO promotes cerebral cortical hyperemia during cortical spreading depression in rabbits ; microspheres; N”-nitro-L-arginine; cerebral blood flow 7-nitroindazole; urethan; TEMPORARY ELEVATIONS in cerebral blood flow (CBF) characterize (CSD) in anesthetized animal models (7, 8, 12, 21, 27, 37). Colonna et al. (3) recently reported, as have others (35), that CSD stimulates the release of calcitonin generelated peptide (CGRP), a potent endogenous vasodilator residing in cerebral perivascular nerves that dilates rabbit pial arterioles (22). In those experiments, however, application of a CGRP-receptor antagonist (the 8to 37-amino acid CGRP fragment) did not completely block dilation of pial arterioles during CSD (3,35). This suggests that there may be additional vasodilator substances released during CSD, with (NO) being a possible cidate. In separate experiments, using an identical pial window technique in rabbits, we topically applied on t.“le brain surface the NO synthase (NOS) inhibitors Arti-nitro-L-arginine methyl ester (L-NAME) 1V’l’nitroL-.arginine (L-NNA), thereby inhibiting pial arteriolar 0363-6135/97 $5.00 Copyright o 1997 dilation during CSD (4, 23). Additional CSD experiments in cats by Wahl et al. (35) provide additional, supportive evidence that NO synthesis modulates pial arteriolar tone during CSD. It is therefore plausible that during CSD, NO could act as a potent modulator not only of pial arteriolar tone but also of CBF. Indeed, a http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Neuronal NO promotes cerebral cortical hyperemia during cortical spreading depression in rabbits

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Publisher
The American Physiological Society
Copyright
Copyright © 1997 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

; microspheres; N”-nitro-L-arginine; cerebral blood flow 7-nitroindazole; urethan; TEMPORARY ELEVATIONS in cerebral blood flow (CBF) characterize (CSD) in anesthetized animal models (7, 8, 12, 21, 27, 37). Colonna et al. (3) recently reported, as have others (35), that CSD stimulates the release of calcitonin generelated peptide (CGRP), a potent endogenous vasodilator residing in cerebral perivascular nerves that dilates rabbit pial arterioles (22). In those experiments, however, application of a CGRP-receptor antagonist (the 8to 37-amino acid CGRP fragment) did not completely block dilation of pial arterioles during CSD (3,35). This suggests that there may be additional vasodilator substances released during CSD, with (NO) being a possible cidate. In separate experiments, using an identical pial window technique in rabbits, we topically applied on t.“le brain surface the NO synthase (NOS) inhibitors Arti-nitro-L-arginine methyl ester (L-NAME) 1V’l’nitroL-.arginine (L-NNA), thereby inhibiting pial arteriolar 0363-6135/97 $5.00 Copyright o 1997 dilation during CSD (4, 23). Additional CSD experiments in cats by Wahl et al. (35) provide additional, supportive evidence that NO synthesis modulates pial arteriolar tone during CSD. It is therefore plausible that during CSD, NO could act as a potent modulator not only of pial arteriolar tone but also of CBF. Indeed, a

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Mar 1, 1997

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