P58. Role of nitrite in neurovascular coupling

Nitric Oxide ◽  
2011 ◽  
Vol 24 ◽  
pp. S37
Author(s):  
Barbora Piknova ◽  
Ara Kocharyan ◽  
Afonso Silva ◽  
Alan N. Schechter
Keyword(s):  
Neurovascular Coupling

scholarly journals The role of nitrite in neurovascular coupling

2011 ◽  
Vol 1407 ◽  
pp. 62-68 ◽  
Author(s):  
Barbora Piknova ◽  
Ara Kocharyan ◽  
Alan N. Schechter ◽  
Afonso C. Silva
Keyword(s):  
Neurovascular Coupling

Role of cerebrovascular autoregulation in neurovascular coupling (Conference Presentation)

2020 ◽  
Author(s):  
Deepshikha Acharya ◽  
Alexander Ruesch ◽  
Jason Yang ◽  
Samantha Schmitt ◽  
Jana M. Kainerstorfer ◽  
...  
Keyword(s):  
Neurovascular Coupling ◽  
Cerebrovascular Autoregulation

The role of sympathetic activation and carbon dioxide tension in human neurovascular coupling

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Ryan E Rosentreter ◽  
Niloofar Mirzadzare ◽  
Woojin Cho ◽  
Michael Potemkin ◽  
Berkeley A Scott ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Neurovascular Coupling ◽  
Carbon Dioxide Tension ◽  
Sympathetic Activation

scholarly journals Key role of tissue plasminogen activator in neurovascular coupling

2008 ◽  
Vol 105 (3) ◽  
pp. 1073-1078 ◽  
Author(s):  
L. Park ◽  
E. F. Gallo ◽  
J. Anrather ◽  
G. Wang ◽  
E. H. Norris ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Neurovascular Coupling ◽  
Tissue Plasminogen

Vascular dysfunction in the brain; implications for heavy metals exposure

2021 ◽  
Vol 17 ◽  
Author(s):  
Nzube F. Olung ◽  
Oritoke M. Aluko ◽  
Sikirullai O. Jeje ◽  
Ayotunde S. Adeagbo ◽  
Omamuyovwi M. Ijomone
Keyword(s):  
Risk Factors ◽  
Heavy Metals ◽  
Vascular Dysfunction ◽  
Neurovascular Unit ◽  
Neurovascular Coupling ◽  
The Brain ◽  
Neurovascular Damage ◽  
Metals Exposure ◽  
Neurovascular Dysfunction

: Normal or diseased conditions that alter the brain’s requirement for oxygen and nutrients via alterations to neurovascular coupling act at the level of the neurovascular unit; comprising neuronal, glial and vascular components. The communications between the components of the neurovascular unit are precise and accurate for its functions, hence a minute disturbance can result in neurovascular dysfunction. Heavy metals such as cadmium, mercury, and lead have been identified to increase the vulnerability of the neurovascular unit to damage. This review examines the role of heavy metals in neurovascular dysfunctions and the possible mechanisms by which these metals act. Risk factors ranging from lifestyle, environment, genetics, infections, and physiologic ageing involved in neurological dysfunctions were highlighted, while stroke, was discussed as the prevalent consequence of neurovascular dysfunctions. Furthermore, the role of these heavy metals in the pathogenesis of stroke consequently pinpoints the importance of understanding the mechanisms of neurovascular damage in a bid to curb the occurrence of neurovascular dysfunctions.

scholarly journals Prostaglandin E2, a Postulated Astrocyte-Derived Neurovascular Coupling Agent, Constricts Rather than Dilates Parenchymal Arterioles

2013 ◽  
Vol 33 (4) ◽  
pp. 479-482 ◽  
Author(s):  
Fabrice Dabertrand ◽  
Rachael M Hannah ◽  
Jessica M Pearson ◽  
David C Hill-Eubanks ◽  
Joseph E Brayden ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Mouse Brain ◽  
Coupling Agent ◽  
Neurovascular Coupling ◽  
Prostaglandin E ◽  
Direct Effects ◽  
Direct Role ◽  
Astrocytic Endfeet

It has been proposed that prostaglandin E2 (PGE2) is released from astrocytic endfeet to dilate parenchymal arterioles through activation of prostanoid (EP4) receptors during neurovascular coupling. However, the direct effects of PGE2 on isolated parenchymal arterioles have not been tested. Here, we examined the effects of PGE2 on the diameter of isolated pressurized parenchymal arterioles from rat and mouse brain. Contrary to the prevailing assumption, we found that PGE2 (0.1, 1, and 5 μmol/L) constricted rather than dilated parenchymal arterioles. Vasoconstriction to PGE2 was prevented by inhibitors of EP1 receptors. These results strongly argue against a direct role of PGE2 on arterioles during neurovascular coupling.

scholarly journals Role of Astrocytes in Neurovascular Coupling

Neuron ◽  
2011 ◽  
Vol 71 (5) ◽  
pp. 782-797 ◽  
Author(s):  
Gabor C. Petzold ◽  
Venkatesh N. Murthy
Keyword(s):  
Neurovascular Coupling

scholarly journals The Role of Endothelial Ca2+ Signaling in Neurovascular Coupling: A View from the Lumen

2018 ◽  
Vol 19 (4) ◽  
pp. 938 ◽  
Author(s):  
Germano Guerra ◽  
Angela Lucariello ◽  
Angelica Perna ◽  
Laura Botta ◽  
Antonio De Luca ◽  
...  
Keyword(s):  
Neurovascular Coupling

scholarly journals Mechanisms Mediating Functional Hyperemia in the Brain

2017 ◽  
Vol 24 (1) ◽  
pp. 73-83 ◽  
Author(s):  
Amy R. Nippert ◽  
Kyle R. Biesecker ◽  
Eric A. Newman
Keyword(s):  
Nitric Oxide ◽  
Arachidonic Acid ◽  
Final Section ◽  
Neurovascular Coupling ◽  
Functional Hyperemia ◽  
Generating Functional ◽  
Signaling Mechanisms ◽  
The Brain ◽  
Astrocyte Endfeet

Neuronal activity within the brain evokes local increases in blood flow, a response termed functional hyperemia. This response ensures that active neurons receive sufficient oxygen and nutrients to maintain tissue function and health. In this review, we discuss the functions of functional hyperemia, the types of vessels that generate the response, and the signaling mechanisms that mediate neurovascular coupling, the communication between neurons and blood vessels. Neurovascular coupling signaling is mediated primarily by the vasoactive metabolites of arachidonic acid (AA), by nitric oxide, and by K+. While much is known about these pathways, many contentious issues remain. We highlight two controversies, the role of glial cell Ca2+ signaling in mediating neurovascular coupling and the importance of capillaries in generating functional hyperemia. We propose signaling pathways that resolve these controversies. In this scheme, capillary dilations are generated by Ca2+ increases in astrocyte endfeet, leading to production of AA metabolites. In contrast, arteriole dilations are generated by Ca2+ increases in neurons, resulting in production of nitric oxide and AA metabolites. Arachidonic acid from neurons also diffuses into astrocyte endfeet where it is converted into additional vasoactive metabolites. While this scheme resolves several discrepancies in the field, many unresolved challenges remain and are discussed in the final section of the review.

Role of Nitrite in Neurovascular Coupling: Possible Nitric Oxiderelated and -independent Mechanisms

2010 ◽  
Vol 49 ◽  
pp. S118
Author(s):  
Barbora Piknova ◽  
Ara Kocharyan ◽  
Afonso Silva ◽  
Alan N Schechter
Keyword(s):  
Neurovascular Coupling
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