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Journal articles on the topic 'Cerebrovascular regulation'

Author: Grafiati

Published: 25 January 2025

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1

Benyó, Zoltán, Éva Ruisanchez, Miriam Leszl-Ishiguro, Péter Sándor, and Pál Pacher. "Endocannabinoids in cerebrovascular regulation." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 7 (April 1, 2016): H785—H801. http://dx.doi.org/10.1152/ajpheart.00571.2015.

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The cerebral blood flow is tightly regulated by myogenic, endothelial, metabolic, and neural mechanisms under physiological conditions, and a large body of recent evidence indicates that inflammatory pathways have a major influence on the cerebral blood perfusion in certain central nervous system disorders, like hemorrhagic and ischemic stroke, traumatic brain injury, and vascular dementia. All major cell types involved in cerebrovascular control pathways (i.e., smooth muscle, endothelium, neurons, astrocytes, pericytes, microglia, and leukocytes) are capable of synthesizing endocannabinoids and/or express some or several of their target proteins [i.e., the cannabinoid 1 and 2 (CB1 and CB2) receptors and the transient receptor potential vanilloid type 1 ion channel]. Therefore, the endocannabinoid system may importantly modulate the regulation of cerebral circulation under physiological and pathophysiological conditions in a very complex manner. Experimental data accumulated since the late 1990s indicate that the direct effect of cannabinoids on cerebral vessels is vasodilation mediated, at least in part, by CB1 receptors. Cannabinoid-induced cerebrovascular relaxation involves both a direct inhibition of smooth muscle contractility and a release of vasodilator mediator(s) from the endothelium. However, under stress conditions (e.g., in conscious restrained animals or during hypoxia and hypercapnia), cannabinoid receptor activation was shown to induce a reduction of the cerebral blood flow, probably via inhibition of the electrical and/or metabolic activity of neurons. Finally, in certain cerebrovascular pathologies (e.g., subarachnoid hemorrhage, as well as traumatic and ischemic brain injury), activation of CB2 (and probably yet unidentified non-CB1/non-CB2) receptors appear to improve the blood perfusion of the brain via attenuating vascular inflammation.

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2

Miller, Stephanie. "NIRS-based cerebrovascular regulation assessment: exercise and cerebrovascular reactivity." Neurophotonics 4, no. 04 (September 12, 2017): 1. http://dx.doi.org/10.1117/1.nph.4.4.041503.

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3

Yang, Yi, David Simpson, Bingren Hu, Jia Liu, and Li Xiong. "Cerebrovascular Regulation in Neurological Disorders." BioMed Research International 2018 (October 8, 2018): 1–2. http://dx.doi.org/10.1155/2018/8140545.

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4

Eisenach, J. C., C. Tong, D. A. Stump, and S. M. Block. "Vasopressin and fetal cerebrovascular regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 2 (August 1, 1992): R376—R381. http://dx.doi.org/10.1152/ajpregu.1992.263.2.r376.

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Vasopressin (AVP) may increase cerebral blood flow (CBF) during hypoxemia by selective dilatation of cerebral vessels via endothelium-derived relaxing factor (EDRF) release. To test whether this action is relevant in the fetus, we produced isocapnic hypoxemia in halothane-anesthetized pregnant ewes. Fetal infusion of a V1 AVP antagonist reduced by 55% the increase in CBF during fetal hypoxemia. To test the role of this response during development, we examined the response to AVP in intact and endothelium-denuded femoral and basilar arterial rings in vitro from fetal, newborn, and adult sheep. AVP constricted femoral rings in an endothelium-independent manner, with increased potency in newborn and fetal compared with adult rings. AVP relaxed basilar rings in an endothelium-dependent manner, which was unaffected by indomethacin treatment, with increased potency in newborn and adult compared with fetal rings. We conclude that fetal cerebral vascular endothelium is functional and responsive to AVP and that circulating AVP during fetal hypoxemia contributes to increased CBF via this effect.

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5

Jafari, Behrouz. "Cerebrovascular Regulation and Sleep Apnea." Current Sleep Medicine Reports 4, no. 3 (July 17, 2018): 196–201. http://dx.doi.org/10.1007/s40675-018-0123-6.

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6

Daffertshofer, M., and M. Hennerici. "Cerebrovascular regulation and vasoneuronal coupling." Journal of Clinical Ultrasound 23, no. 2 (February 1995): 125–38. http://dx.doi.org/10.1002/jcu.1870230207.

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7

Caldwell, Hannah G., Jay M. J. R. Carr, Jatinder S. Minhas, Erik R. Swenson, and Philip N. Ainslie. "Acid–base balance and cerebrovascular regulation." Journal of Physiology 599, no. 24 (November 26, 2021): 5337–59. http://dx.doi.org/10.1113/jp281517.

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8

Koehler, Raymond C., Debebe Gebremedhin, and David R. Harder. "Role of astrocytes in cerebrovascular regulation." Journal of Applied Physiology 100, no. 1 (January 2006): 307–17. http://dx.doi.org/10.1152/japplphysiol.00938.2005.

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Astrocytes send processes to synapses and blood vessels, communicate with other astrocytes through gap junctions and by release of ATP, and thus are an integral component of the neurovascular unit. Electrical field stimulations in brain slices demonstrate an increase in intracellular calcium in astrocyte cell bodies transmitted to perivascular end-feet, followed by a decrease in vascular smooth muscle calcium oscillations and arteriolar dilation. The increase in astrocyte calcium after neuronal activation is mediated, in part, by activation of metabotropic glutamate receptors. Calcium signaling in vitro can also be influenced by adenosine acting on A2B receptors and by epoxyeicosatrienoic acids (EETs) shown to be synthesized in astrocytes. Prostaglandins, EETs, arachidonic acid, and potassium ions are candidate mediators of communication between astrocyte end-feet and vascular smooth muscle. In vivo evidence supports a role for cyclooxygenase-2 metabolites, EETs, adenosine, and neuronally derived nitric oxide in the coupling of increased blood flow to increased neuronal activity. Combined inhibition of the EETs, nitric oxide, and adenosine pathways indicates that signaling is not by parallel, independent pathways. Indirect pharmacological results are consistent with astrocytes acting as intermediaries in neurovascular signaling within the neurovascular unit. For specific stimuli, astrocytes are also capable of transmitting signals to pial arterioles on the brain surface for ensuring adequate inflow pressure to parenchymal feeding arterioles. Therefore, evidence from brain slices and indirect evidence in vivo with pharmacological approaches suggest that astrocytes play a pivotal role in regulating the fundamental physiological response coupling dynamic changes in cerebral blood flow to neuronal synaptic activity. Future work using in vivo imaging and genetic manipulation will be required to provide more direct evidence for a role of astrocytes in neurovascular coupling.

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9

Raz, Limor. "Estrogen and cerebrovascular regulation in menopause." Molecular and Cellular Endocrinology 389, no. 1-2 (May 2014): 22–30. http://dx.doi.org/10.1016/j.mce.2014.01.015.

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10

Edvinsson, L. "Cerebrovascular gene regulation in brain diseases." Journal of the Neurological Sciences 283, no. 1-2 (August 2009): 246. http://dx.doi.org/10.1016/j.jns.2009.02.032.

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11

Del Toro, Jorge, Penelope T. Louis, and Jan Goddard-Finegold. "Cerebrovascular regulation and neonatal brain injury." Pediatric Neurology 7, no. 1 (January 1991): 3–12. http://dx.doi.org/10.1016/0887-8994(91)90098-6.

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12

Van Skike, Candice E., and Veronica Galvan. "A Perfect sTORm: The Role of the Mammalian Target of Rapamycin (mTOR) in Cerebrovascular Dysfunction of Alzheimer's Disease: A Mini-Review." Gerontology 64, no. 3 (2018): 205–11. http://dx.doi.org/10.1159/000485381.

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Cerebrovascular dysfunction is detected prior to the onset of cognitive and histopathological changes in Alzheimer's disease (AD). Increasing evidence indicates a critical role of cerebrovascular dysfunction in the initiation and progression of AD. Recent studies identified the mechanistic/mammalian target of rapamycin (mTOR) as a critical effector of cerebrovascular dysfunction in AD. mTOR has a key role in the regulation of metabolism, but some mTOR-dependent mechanisms are uniquely specific to the regulation of cerebrovascular function. These include the regulation of cerebral blood flow, blood-brain barrier integrity and maintenance, neurovascular coupling, and cerebrovascular reactivity. This article examines the available evidence for a role of mTOR-driven cerebrovascular dysfunction in the pathogenesis of AD and of vascular cognitive impairment and dementia (VCID) and highlights the therapeutic potential of targeting mTOR and/or specific downstream effectors for vasculoprotection in AD, VCID, and other age-associated neurological diseases with cerebrovascular etiology.

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13

Guadagni, Veronica, Lauren L. Drogos, Amanda V. Tyndall, Margie H. Davenport, Todd J. Anderson, Gail A. Eskes, R. Stewart Longman, Michael D. Hill, David B. Hogan, and Marc J. Poulin. "Aerobic exercise improves cognition and cerebrovascular regulation in older adults." Neurology 94, no. 21 (May 13, 2020): e2245-e2257. http://dx.doi.org/10.1212/wnl.0000000000009478.

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ObjectiveTo test the hypothesis that aerobic exercise is associated with improvements in cognition and cerebrovascular regulation, we enrolled 206 healthy low-active middle-aged and older adults (mean ± SD age 65.9 ± 6.4 years) in a supervised 6-month aerobic exercise intervention and assessed them before and after the intervention.MethodsThe study is a quasi-experimental single group pre/postintervention study. Neuropsychological tests were used to assess cognition before and after the intervention. Transcranial Doppler ultrasound was used to measure cerebral blood flow velocity. Cerebrovascular regulation was assessed at rest, during euoxic hypercapnia, and in response to submaximal exercise. Multiple linear regression was used to examine the association between changes in cognition and changes in cerebrovascular function.ResultsThe intervention was associated with improvements in some cognitive domains, cardiorespiratory fitness, and cerebrovascular regulation. Changes in executive functions were negatively associated with changes in cerebrovascular resistance index (CVRi) during submaximal exercise (β = −0.205, p = 0.013), while fluency improvements were positively associated with changes in CVRi during hypercapnia (β = 0.106, p = 0.03).ConclusionThe 6-month aerobic exercise intervention was associated with improvements in some cognitive domains and cerebrovascular regulation. Secondary analyses showed a novel association between changes in cognition and changes in cerebrovascular regulation during euoxic hypercapnia and in response to submaximal exercise.

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14

Boedtkjer, Ebbe. "Acid–base regulation and sensing: Accelerators and brakes in metabolic regulation of cerebrovascular tone." Journal of Cerebral Blood Flow & Metabolism 38, no. 4 (October 6, 2017): 588–602. http://dx.doi.org/10.1177/0271678x17733868.

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Metabolic regulation of cerebrovascular tone directs blood flow to areas of increased neuronal activity and during disease states partially compensates for insufficient perfusion by enhancing blood flow in collateral blood vessels. Acid–base disturbances frequently occur as result of enhanced metabolism or insufficient blood supply, but despite definitive evidence that acid–base disturbances alter arterial tone, effects of individual acid–base equivalents and the underlying signaling mechanisms are still being debated. H+ is an important intra- and extracellular messenger that modifies cerebrovascular tone. In addition, low extracellular [HCO3–] promotes cerebrovascular contraction through an endothelium-dependent mechanism. CO2 alters arterial tone development via changes in intra- and extracellular pH but it is still controversial whether CO2 also has direct vasomotor effects. Vasocontractile responses to low extracellular [HCO3–] and acute CO2-induced decreases in intracellular pH can counteract H+-mediated vasorelaxation during metabolic and respiratory acidosis, respectively, and may thereby reduce the risk of capillary damage and cerebral edema that could be consequences of unopposed vasodilation. In this review, the signaling mechanisms for acid–base equivalents in cerebral arteries and the mechanisms of intracellular pH control in the arterial wall are discussed in the context of metabolic regulation of cerebrovascular tone and local perfusion.

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15

Webb, Alastair J. S., Elizabeth B. Klerman, and Emiri T. Mandeville. "Circadian and Diurnal Regulation of Cerebral Blood Flow." Circulation Research 134, no. 6 (March 15, 2024): 695–710. http://dx.doi.org/10.1161/circresaha.123.323049.

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Circadian and diurnal variation in cerebral blood flow directly contributes to the diurnal variation in the risk of stroke, either through factors that trigger stroke or due to impaired compensatory mechanisms. Cerebral blood flow results from the integration of systemic hemodynamics, including heart rate, cardiac output, and blood pressure, with cerebrovascular regulatory mechanisms, including cerebrovascular reactivity, autoregulation, and neurovascular coupling. We review the evidence for the circadian and diurnal variation in each of these mechanisms and their integration, from the detailed evidence for mechanisms underlying the nocturnal nadir and morning surge in blood pressure to identifying limited available evidence for circadian and diurnal variation in cerebrovascular compensatory mechanisms. We, thus, identify key systemic hemodynamic factors related to the diurnal variation in the risk of stroke but particularly identify the need for further research focused on cerebrovascular regulatory mechanisms.

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16

Morton, Jude S., Breanna Patton, Cameron J. Morse, Zeyad El Karsh, Lucas A. Rodrigues, Darrell D. Mousseau, David P. Ferguson, Daniel A. Columbus, Lynn P. Weber, and T. Dylan Olver. "Altered cerebrovascular regulation in low birthweight swine." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 267 (May 2022): 111163. http://dx.doi.org/10.1016/j.cbpa.2022.111163.

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17

Iadecola, Costantino, Dale A. Pelligrino, Michael A. Moskowitz, and Niels A. Lassen. "Nitric Oxide Synthase Inhibition and Cerebrovascular Regulation." Journal of Cerebral Blood Flow & Metabolism 14, no. 2 (March 1994): 175–92. http://dx.doi.org/10.1038/jcbfm.1994.25.

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There is increasing evidence that nitric oxide (NO) is an important molecular messenger involved in a wide variety of biological processes. Recent data suggest that NO is also involved in the regulation of the cerebral circulation. Thus, NO participants in the maintenance of resting cerebrovascular tone and may play an important role in selected vasodilator responses of the cerebral circulation. Furthermore, evidence has been presented suggesting that NO participates in the mechanisms of cerebral ischemic damage. Despite the widespread attention that NO has captured in recent years and the large number of studies that have been published on the subject, there is considerable controversy regarding the role of this agent in cerebrovascular regulation and in ischemic damage. In this paper the results of investigations on NO and the cerebral circulation are reviewed and the evidence for and against a role of NO is critically examined.

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18

Toda, Noboru. "Nitrergic cerebrovascular regulation as affected by donepezil." Folia Pharmacologica Japonica 141, no. 3 (2013): 150–54. http://dx.doi.org/10.1254/fpj.141.150.

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19

Silpanisong, Jinjutha, and William Pearce. "Vasotrophic Regulation of Age-Dependent Hypoxic Cerebrovascular Remodeling." Current Vascular Pharmacology 11, no. 5 (August 31, 2013): 544–63. http://dx.doi.org/10.2174/1570161111311050002.

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20

Gebremedhin, Debebe, Sandeep Gopalakrishnan, and David Harder. "Endogenous Events Modulating Myogenic Regulation of Cerebrovascular Function." Current Vascular Pharmacology 12, no. 6 (December 10, 2014): 810–17. http://dx.doi.org/10.2174/15701611113116660153.

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21

N. Atochin, Dmitriy, and Paul L. Huang. "Role of Endothelial Nitric Oxide in Cerebrovascular Regulation." Current Pharmaceutical Biotechnology 12, no. 9 (September 1, 2011): 1334–42. http://dx.doi.org/10.2174/138920111798280974.

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22

Morgan, Barbara J., Kevin J. Reichmuth, Paul E. Peppard, Laurel Finn, Steven R. Barczi, Terry Young, and F. Javier Nieto. "Effects of Sleep-disordered Breathing on Cerebrovascular Regulation." American Journal of Respiratory and Critical Care Medicine 182, no. 11 (December 2010): 1445–52. http://dx.doi.org/10.1164/rccm.201002-0313oc.

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23

Shoemaker, Leena N., Luke C. Wilson, Samuel J. E. Lucas, Liana Machado, and James D. Cotter. "Cerebrovascular regulation is not blunted during mental stress." Experimental Physiology 104, no. 11 (October 9, 2019): 1678–87. http://dx.doi.org/10.1113/ep087832.

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24

Raignault, Adeline, Virginie Bolduc, Frédéric Lesage, and Eric Thorin. "Pulse pressure-dependent cerebrovascular eNOS regulation in mice." Journal of Cerebral Blood Flow & Metabolism 37, no. 2 (July 21, 2016): 413–24. http://dx.doi.org/10.1177/0271678x16629155.

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Arterial blood pressure is oscillatory; whether pulse pressure (PP) regulates cerebral artery myogenic tone (MT) and endothelial function is currently unknown. To test the impact of PP on MT and dilation to flow (FMD) or to acetylcholine (Ach), isolated pressurized mouse posterior cerebral arteries were subjected to either static pressure (SP) or a physiological PP (amplitude: 30 mm Hg; frequency: 550 bpm). Under PP, MT was significantly higher than in SP conditions ( p < 0.05) and was not affected by eNOS inhibition. In contrast, under SP, eNOS inhibition increased ( p < 0.05) MT to levels observed under PP, suggesting that PP may inhibit eNOS. At a shear stress of 20 dyn/cm2, FMD was lower ( p < 0.05) under SP than PP. Under SP, eNOS-dependent [Formula: see text] production contributed to FMD, while under PP, eNOS-dependent NO was responsible for FMD, indicating that PP favours eNOS coupling. Differences in FMD between pressure conditions were abolished after NOX2 inhibition. In contrast to FMD, Ach-induced dilations were higher ( p < 0.05) under SP than PP. Reactive oxygen species scavenging reduced ( p < 0.05) Ach-dependent dilations under SP, but increased ( p < 0.05) them under PP; hence, under PP, Ach promotes ROS production and limits eNOS-derived NO activity. In conclusion, PP finely regulates eNOS, controlling cerebral artery reactivity.

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Willie, Christopher K. "Uncoupling neurovascular coupling: putative pathways of cerebrovascular regulation?" Journal of Applied Physiology 115, no. 8 (October 15, 2013): 1215. http://dx.doi.org/10.1152/japplphysiol.00813.2013.

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26

Hamel, Edith. "Perivascular nerves and the regulation of cerebrovascular tone." Journal of Applied Physiology 100, no. 3 (March 2006): 1059–64. http://dx.doi.org/10.1152/japplphysiol.00954.2005.

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Brain perfusion is tightly coupled to neuronal activity, is commonly used to monitor normal or pathological brain function, and is a direct reflection of the interactions that occur between neuronal signals and blood vessels. Cerebral blood vessels at the surface and within the brain are surrounded by nerve fibers that originate, respectively, from peripheral nerve ganglia and intrinsic brain neurons. Although of different origin and targeting distinct vascular beds, these “perivascular nerves” fulfill similar roles related to cerebrovascular functions, a major one being to regulate their tone and, therein, brain perfusion. This utmost function, which underlies the signals used in functional neuroimaging techniques and which can be jeopardized in pathologies such as Alzheimer's disease, stroke, and migraine headache, is thus regulated at several levels. Recently, new insights into our understanding of how neural input regulate cerebrovascular tone resulted in the rediscovery of the functional “neurovascular unit.” These remarkable advances suggest that neuron-driven changes in vascular tone result from interactions that involve all components of the neurovascular unit, transducing neuronal signals into vasomotor responses not only through direct interaction between neurons and vessels but also indirectly via the perivascular astrocytes. Neurovascular coupling is thus determined by chemical signals released from activated perivascular nerves and astrocytes that alter vascular tone to locally adjust perfusion to the spatial and temporal changes in brain activity.

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27

Tan, C. O., W. P. Meehan, G. L. Iverson, and J. A. Taylor. "Cerebrovascular regulation, exercise, and mild traumatic brain injury." Neurology 83, no. 18 (October 1, 2014): 1665–72. http://dx.doi.org/10.1212/wnl.0000000000000944.

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Edvinsson, Lars. "Cerebrovascular Angiotensin AT1 Receptor Regulation in Cerebral Ischemia." Trends in Cardiovascular Medicine 18, no. 3 (April 2008): 98–103. http://dx.doi.org/10.1016/j.tcm.2008.01.005.

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29

Kempski, O., M. Spatz, G. Valet, and A. Baethmann. "Cell volume regulation of cerebrovascular endothelium in vitro." Journal of Cellular Physiology 123, no. 1 (April 1985): 51–54. http://dx.doi.org/10.1002/jcp.1041230109.

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30

Marshall, Olga, Sanjeev Chawla, Hanzhang Lu, Louise Pape, and Yulin Ge. "Cerebral blood flow modulation insufficiency in brain networks in multiple sclerosis: A hypercapnia MRI study." Journal of Cerebral Blood Flow & Metabolism 36, no. 12 (July 20, 2016): 2087–95. http://dx.doi.org/10.1177/0271678x16654922.

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Cerebrovascular reactivity measures vascular regulation of cerebral blood flow and is responsible for maintaining healthy neurovascular coupling. Multiple sclerosis exhibits progressive neurodegeneration and global cerebrovascular reactivity deficits. This study investigates varied degrees of cerebrovascular reactivity impairment in different brain networks, which may be an underlying cause for functional changes in the brain, affecting long-distance projection integrity and cognitive function; 28 multiple sclerosis and 28 control subjects underwent pseudocontinuous arterial spin labeling perfusion MRI to measure cerebral blood flow under normocapnia (room air) and hypercapnia (5% carbon dioxide gas mixture) breathing. Cerebrovascular reactivity, measured as normocapnic to hypercapnic cerebral blood flow percent increase normalized by end-tidal carbon dioxide change, was determined from seven functional networks (default mode, frontoparietal, somatomotor, visual, limbic, dorsal, and ventral attention networks). Group analysis showed significantly decreased cerebrovascular reactivity in patients compared to controls within the default mode, frontoparietal, somatomotor, and ventral attention networks after multiple comparison correction. Regression analysis showed a significant correlation of cerebrovascular reactivity with lesion load in the default mode and ventral attention networks and with gray matter atrophy in the default mode network. Functional networks in multiple sclerosis patients exhibit varied amounts of cerebrovascular reactivity deficits. Such blood flow regulation abnormalities may contribute to functional communication disruption in multiple sclerosis.

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31

Salles, Antonio A. F. de. "The role of the endothelial dependent relaxing factor in the regulation of cerebral circulation." Arquivos de Neuro-Psiquiatria 46, no. 1 (March 1988): 90–97. http://dx.doi.org/10.1590/s0004-282x1988000100016.

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It has recently been demonstrated that vessel dilation induced by several physiological agents is dependent on an intact vascular endothelium. In order to explain this endothelium dependence, it has been hypothesized that a still unknown chemical substance, generically named Endothelium Dependent Relaxing Factor (EDRF) is necessary for physiological vasodilation. The role of this EDRF in the cerebrovascular physiology is not yet well understood. In this article the cerebrovascular physiological control is reviewed in relationship with possible EDRF actions. The importance of endothelial lesions in the cerebrovascular responses is discussed.

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32

Sprick, Justin D., Joe R. Nocera, Ihab Hajjar, W. Charles O’Neill, James Bailey, and Jeanie Park. "Cerebral blood flow regulation in end-stage kidney disease." American Journal of Physiology-Renal Physiology 319, no. 5 (November 1, 2020): F782—F791. http://dx.doi.org/10.1152/ajprenal.00438.2020.

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Patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD) experience an increased risk of cerebrovascular disease and cognitive dysfunction. Hemodialysis (HD), a major modality of renal replacement therapy in ESKD, can cause rapid changes in blood pressure, osmolality, and acid-base balance that collectively present a unique stress to the cerebral vasculature. This review presents an update regarding cerebral blood flow (CBF) regulation in CKD and ESKD and how the maintenance of cerebral oxygenation may be compromised during HD. Patients with ESKD exhibit decreased cerebral oxygen delivery due to anemia, despite cerebral hyperperfusion at rest. Cerebral oxygenation further declines during HD due to reductions in CBF, and this may induce cerebral ischemia or “stunning.” Intradialytic reductions in CBF are driven by decreases in cerebral perfusion pressure that may be partially opposed by bicarbonate shifts during dialysis. Intradialytic reductions in CBF have been related to several variables that are routinely measured in clinical practice including ultrafiltration rate and blood pressure. However, the role of compensatory cerebrovascular regulatory mechanisms during HD remains relatively unexplored. In particular, cerebral autoregulation can oppose reductions in CBF driven by reductions in systemic blood pressure, while cerebrovascular reactivity to CO2 may attenuate intradialytic reductions in CBF through promoting cerebral vasodilation. However, whether these mechanisms are effective in ESKD and during HD remain relatively unexplored. Important areas for future work include investigating potential alterations in cerebrovascular regulation in CKD and ESKD and how key regulatory mechanisms are engaged and integrated during HD to modulate intradialytic declines in CBF.

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33

Daley, Michael L., Nithya Narayanan, and Charles W. Leffler. "Model-derived assessment of cerebrovascular resistance and cerebral blood flow following traumatic brain injury." Experimental Biology and Medicine 235, no. 4 (April 2010): 539–45. http://dx.doi.org/10.1258/ebm.2010.009253.

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The published guidelines point out the need for the development of methods that individualize patient cerebral perfusion management and minimize secondary ischemic complications associated with traumatic brain injury. A laboratory method has been developed to determine model-derived assessments of cerebrovascular resistance (mCVR) and cerebral blood flow (mCBF) from cerebrovascular pressure transmission, and the dynamic relationship between arterial blood pressure (ABP) and intracranial pressure (ICP). The aim of this two-fold study is to (1) evaluate relative changes in the model-derived parameters of mCVR and mCBF with the corresponding changes in the pial arteriolar vascular parameters of pial arteriolar resistance (PAR) and relative pial arteriolar blood flow (rPABF); and (2) examine the efficacy of the proposed modeling methodology for continuous assessment of the state of cerebrovascular regulation by evaluating relative changes in the model-derived parameters of CBF and cerebrovascular resistance in relation to changes of cerebral perfusion pressure prior to and following fluid percussion brain injury. Changes of ABP, ICP, PAR, relative arteriolar blood flow (rPABF) and the corresponding model-derived parameters of mCBF and mCVR induced by acute hypertensive challenge were evaluated before and following fluid percussion injury in piglets equipped with cranial windows. Before fluid percussion, hypertensive challenge resulted in a significant increase of PAR and mCVR, whereas both rPABF and mCBF remained constant. Following fluid percussion, hypertensive challenge resulted in a significant decrease of PAR and mCVR and consistent with impaired cerebrovascular regulation. Hypertensive challenge significantly increased both rPABF and mCBF, which approximately doubled with increased CPP with correlation values of r = 0.96 ( P < 0.01) and r = 0.97 ( P ≤ 0.01), respectively. The assessment of model-derived cerebrovascular resistance and CBF with changes of CPP provides a means to monitor continuously the state of cerebrovascular regulation.

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34

Sugawara, Jun, Takeshi Hashimoto, Hayato Tsukamoto, Niels H. Secher, and Shigehiko Ogoh. "Cerebrovascular Regulation In Response To High-intensity Interval Exercise." Medicine & Science in Sports & Exercise 54, no. 9S (September 2022): 450. http://dx.doi.org/10.1249/01.mss.0000880704.30831.5f.

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35

Tan, Can Ozan, J. W. Hamner, and J. Andrew Taylor. "The role of myogenic mechanisms in human cerebrovascular regulation." Journal of Physiology 591, no. 20 (September 19, 2013): 5095–105. http://dx.doi.org/10.1113/jphysiol.2013.259747.

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36

Uchiyama, Shinichiro, Tomomi Nakamura, Masako Yamazaki, and Makoto Iwata. "Platelet Activation and Its Regulation in Ischemic Cerebrovascular Disease." Nosotchu 21, no. 4 (1999): 457–62. http://dx.doi.org/10.3995/jstroke.21.4_457.

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37

McCulloch, J., R. Uddman, T. A. Kingman, and L. Edvinsson. "Calcitonin gene-related peptide: functional role in cerebrovascular regulation." Proceedings of the National Academy of Sciences 83, no. 15 (August 1, 1986): 5731–35. http://dx.doi.org/10.1073/pnas.83.15.5731.

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Low, Phillip A., Vera Novak, Judith M. Spies, Peter Novak, and George W. Petty. "Cerebrovascular Regulation in the Postural Orthostatic Tachycardia Syndrome (POTS)." American Journal of the Medical Sciences 317, no. 2 (February 1999): 124–33. http://dx.doi.org/10.1016/s0002-9629(15)40486-0.

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39

Tzeng, Yu-Chieh, Chris K. Willie, Greg Atkinson, Samuel J. E. Lucas, Aaron Wong, and Philip N. Ainslie. "Cerebrovascular Regulation During Transient Hypotension and Hypertension in Humans." Hypertension 56, no. 2 (August 2010): 268–73. http://dx.doi.org/10.1161/hypertensionaha.110.152066.

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Perdomo, Sophy J., Jaimie Ward, Yumei Liu, Eric D. Vidoni, Emily Witte, Jason F. Sisante, Kiersten Kirkendoll, Jeffrey Burns, and Sandra A. Billinger. "Cardiovascular Disease Risk Influences Cerebrovascular Regulation in Older Adults." Medicine & Science in Sports & Exercise 51, Supplement (June 2019): 1–2. http://dx.doi.org/10.1249/01.mss.0000560494.36855.02.

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LOW, PHILLIP A., VERA NOVAK, JUDITH M. SPIES, PETER NOVAK, and GEORGE W. PETTY. "Cerebrovascular Regulation in the Postural Orthostatic Tachycardia Syndrome (POTS)." American Journal of the Medical Sciences 317, no. 2 (February 1999): 124–33. http://dx.doi.org/10.1097/00000441-199902000-00007.

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Hoiland, Ryan L., Connor A. Howe, Geoff B. Coombs, and Philip N. Ainslie. "Ventilatory and cerebrovascular regulation and integration at high-altitude." Clinical Autonomic Research 28, no. 4 (March 24, 2018): 423–35. http://dx.doi.org/10.1007/s10286-018-0522-2.

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Ainslie, Philip N., and James Duffin. "Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 5 (May 2009): R1473—R1495. http://dx.doi.org/10.1152/ajpregu.91008.2008.

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Cerebral blood flow (CBF) and its distribution are highly sensitive to changes in the partial pressure of arterial CO2 (PaCO2). This physiological response, termed cerebrovascular CO2 reactivity, is a vital homeostatic function that helps regulate and maintain central pH and, therefore, affects the respiratory central chemoreceptor stimulus. CBF increases with hypercapnia to wash out CO2 from brain tissue, thereby attenuating the rise in central Pco2, whereas hypocapnia causes cerebral vasoconstriction, which reduces CBF and attenuates the fall of brain tissue Pco2. Cerebrovascular reactivity and ventilatory response to PaCO2 are therefore tightly linked, so that the regulation of CBF has an important role in stabilizing breathing during fluctuating levels of chemical stimuli. Indeed, recent reports indicate that cerebrovascular responsiveness to CO2, primarily via its effects at the level of the central chemoreceptors, is an important determinant of eupneic and hypercapnic ventilatory responsiveness in otherwise healthy humans during wakefulness, sleep, and exercise and at high altitude. In particular, reductions in cerebrovascular responsiveness to CO2 that provoke an increase in the gain of the chemoreflex control of breathing may underpin breathing instability during central sleep apnea in patients with congestive heart failure and on ascent to high altitude. In this review, we summarize the major factors that regulate CBF to emphasize the integrated mechanisms, in addition to PaCO2, that control CBF. We discuss in detail the assessment and interpretation of cerebrovascular reactivity to CO2. Next, we provide a detailed update on the integration of the role of cerebrovascular CO2 reactivity and CBF in regulation of chemoreflex control of breathing in health and disease. Finally, we describe the use of a newly developed steady-state modeling approach to examine the effects of changes in CBF on the chemoreflex control of breathing and suggest avenues for future research.

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Capone, Carmen, Giuseppe Faraco, Laibaik Park, Xian Cao, Robin L. Davisson, and Costantino Iadecola. "The cerebrovascular dysfunction induced by slow pressor doses of angiotensin II precedes the development of hypertension." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 1 (January 2011): H397—H407. http://dx.doi.org/10.1152/ajpheart.00679.2010.

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Hypertension alters cerebrovascular regulation and increases the brain's susceptibility to stroke and dementia. We investigated the temporal relationships between the arterial pressure (AP) elevation induced by “slow pressor” angiotensin II (ANG II) infusion, which recapitulates key features of human hypertension, and the resulting cerebrovascular dysfunction. Minipumps delivering saline or ANG II for 14 days were implanted subcutaneously in C57BL/6 mice ( n = 5/group). Cerebral blood flow was assessed by laser-Doppler flowmetry in anesthetized mice equipped with a cranial window. With ANG II (600 ng·kg−1·min−1), AP started to rise after 9 days ( P < 0.05 vs. saline), remained elevated at 11–17 days, and returned to baseline at 21 days ( P > 0.05). ANG II attenuated the cerebral blood flow increase induced by neural activity (whisker stimulation) or endothelium-dependent vasodilators, an effect observed before the AP elevation (7 days), as well as after the hypertension subsided (21 days). Nonpressor doses of ANG II (200 ng·kg−1·min−1) induced cerebrovascular dysfunction and oxidative stress without elevating AP ( P > 0.05 vs. saline), whereas phenylephrine elevated AP without inducing cerebrovascular effects. ANG II (600 ng·kg−1·min−1) augmented neocortical reactive oxygen species (ROS) with a time course similar to that of the cerebrovascular dysfunction. Neocortical application of the ROS scavenger manganic(I-II)meso-tetrakis(4-benzoic acid)porphyrin or the NADPH oxidase peptide inhibitor gp91ds-tat attenuated ROS and cerebrovascular dysfunction. We conclude that the alterations in neurovascular regulation induced by slow pressor ANG II develop before hypertension and persist beyond AP normalization but are not permanent. The findings unveil a striking susceptibility of cerebrovascular function to the deleterious effects of ANG II and raise the possibility that cerebrovascular dysregulation precedes the elevation in AP also in patients with ANG II-dependent hypertension.

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Faraco, Giuseppe, Teodora Stella Wijasa, Laibaik Park, Jamie Moore, Joseph Anrather, and Costantino Iadecola. "Water Deprivation Induces Neurovascular and Cognitive Dysfunction through Vasopressin-Induced Oxidative Stress." Journal of Cerebral Blood Flow & Metabolism 34, no. 5 (February 12, 2014): 852–60. http://dx.doi.org/10.1038/jcbfm.2014.24.

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Adequate hydration is essential for normal brain function and dehydration induces cognitive deterioration. In addition, dehydration has emerged as a stroke risk factor. However, it is unknown whether alterations in cerebrovascular regulation are responsible for these effects. To address this issue, C57BI/6 mice were water deprived for 24 or 48 hours and somatosensory cortex blood flow was assessed by laser-Doppler flowmetry in a cranial window. Dehydration increased plasma osmolality and vasopressin levels, and suppressed the increase in blood flow induced by neural activity, by the endothelium-dependent vasodilator acetylcholine and the smooth muscle relaxant adenosine. The cerebrovascular dysfunction was associated with oxidative stress and cognitive deficits, assessed using the Y maze. The vasopressin la receptor antagonist SR49059 improved the dehydration-induced oxidative stress and vasomotor dysfunction. Dehydration upregulated endothelin-1 in cerebral blood vessels, an effect blocked by SR49059. Furthermore, the endothelin A receptor antagonist BQ123 ameliorated cerebrovascular function. These findings show for the first time that dehydration alters critical mechanisms regulating the cerebral circulation through vasopressin and oxidative stress. The ensuing cerebrovascular dysregulation may alter cognitive function and increase the brain's susceptibility to cerebral ischemia.

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Chen, Li, Bin Zhang, Lu Yang, Yun-Gang Bai, Ji-Bo Song, Yi-Ling Ge, Hong-Zhe Ma, Jiu-Hua Cheng, Jin Ma, and Man-Jiang Xie. "BMAL1 Disrupted Intrinsic Diurnal Oscillation in Rat Cerebrovascular Contractility of Simulated Microgravity Rats by Altering Circadian Regulation of miR-103/CaV1.2 Signal Pathway." International Journal of Molecular Sciences 20, no. 16 (August 14, 2019): 3947. http://dx.doi.org/10.3390/ijms20163947.

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The functional and structural adaptations in cerebral arteries could be one of the fundamental causes in the occurrence of orthostatic intolerance after space flight. In addition, emerging studies have found that many cardiovascular functions exhibit circadian rhythm. Several lines of evidence suggest that space flight might increase an astronaut’s cardiovascular risks by disrupting circadian rhythm. However, it remains unknown whether microgravity disrupts the diurnal variation in vascular contractility and whether microgravity impacts on circadian clock system. Sprague-Dawley rats were subjected to 28-day hindlimb-unweighting to simulate the effects of microgravity on vasculature. Cerebrovascular contractility was estimated by investigating vasoconstrictor responsiveness and myogenic tone. The circadian regulation of CaV1.2 channel was determined by recording whole-cell currents, evaluating protein and mRNA expressions. Then the candidate miRNA in relation with Ca2+ signal was screened. Lastly, the underlying pathway involved in circadian regulation of cerebrovascular contractility was determined. The major findings of this study are: (1) The clock gene BMAL1 could induce the expression of miR-103, and in turn modulate the circadian regulation of CaV1.2 channel in rat cerebral arteries at post-transcriptional level; and (2) simulated microgravity disrupted intrinsic diurnal oscillation in rat cerebrovascular contractility by altering circadian regulation of BMAL1/miR-103/CaV1.2 signal pathway.

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Olufsen, Mette S., Ali Nadim, and Lewis A. Lipsitz. "Dynamics of cerebral blood flow regulation explained using a lumped parameter model." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 2 (February 1, 2002): R611—R622. http://dx.doi.org/10.1152/ajpregu.00285.2001.

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The dynamic cerebral blood flow response to sudden hypotension during posture change is poorly understood. To better understand the cardiovascular response to hypotension, we used a windkessel model with two resistors and a capacitor to reproduce beat-to-beat changes in middle cerebral artery blood flow velocity (transcranial Doppler measurements) in response to arterial pressure changes measured in the finger (Finapres). The resistors represent lumped systemic and peripheral resistances in the cerebral vasculature, whereas the capacitor represents a lumped systemic compliance. Ten healthy young subjects were studied during posture change from sitting to standing. Dynamic variations of the peripheral and systemic resistances were extracted from the data on a beat-to-beat basis. The model shows an initial increase, followed approximately 10 s later by a decline in cerebrovascular resistance. The model also suggests that the initial increase in cerebrovascular resistance can explain the widening of the cerebral blood flow pulse observed in young subjects. This biphasic change in cerebrovascular resistance is consistent with an initial vasoconstriction, followed by cerebral autoregulatory vasodilation.

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Matenchuk, Brittany A., Marina James, Rachel J. Skow, Paige Wakefield, Christina MacKay, Craig D. Steinback, and Margie H. Davenport. "Longitudinal study of cerebral blood flow regulation during exercise in pregnancy." Journal of Cerebral Blood Flow & Metabolism 40, no. 11 (November 21, 2019): 2278–88. http://dx.doi.org/10.1177/0271678x19889089.

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Cerebrovascular adaptation to pregnancy is poorly understood. We sought to assess cerebrovascular regulation in response to visual stimulation, hypercapnia and exercise across the three trimesters of pregnancy. Using transcranial Doppler (TCD) ultrasound, middle and posterior cerebral artery mean blood velocities (MCAvmean and PCAvmean) were measured continuously at rest and in response to (1) visual stimulation to assess neurovascular coupling (NVC); (2) a modified Duffin hyperoxic CO2 rebreathe test, and (3) an incremental cycling exercise test to volitional fatigue in non-pregnant ( n = 26; NP) and pregnant women (ﬁrst trimester [ n = 13; TM1], second trimester [ n = 21; TM2], and third trimester [ n = 20; TM3]) in total 47 women. At rest, MCAvmean and PETCO2 were lower in TM2 compared to NP. PCAvmean was lower in TM2 but not TM1 or TM3 compared to NP. Cerebrovascular reactivity in MCAvmean and PCAvmean during the hypercapnic rebreathing test was not different between pregnant and non-pregnant women. MCAvmean continued to increase over the second half of the exercise test in TM2 and TM3, while it decreased in NP due to differences in ΔPETCO2 between groups. Pregnant women experienced a delayed decrease in MCAvmean in response to maximal exercise compared to non-pregnant controls which was explained by CO2 reactivity and PETCO2 level.

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Dongó, Eleni, and Levente Kiss. "The Potential Role of Hydrogen Sulfide in the Regulation of Cerebrovascular Tone." Biomolecules 10, no. 12 (December 16, 2020): 1685. http://dx.doi.org/10.3390/biom10121685.

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A better understanding of the regulation of cerebrovascular circulation is of great importance because stroke and other cerebrovascular diseases represent a major concern in healthcare leading to millions of deaths yearly. The circulation of the central nervous system is regulated in a highly complex manner involving many local factors and hydrogen sulfide (H2S) is emerging as one such possible factor. Several lines of evidence support that H2S takes part in the regulation of vascular tone. Examinations using either exogenous treatment with H2S donor molecules or alterations to the enzymes that are endogenously producing this molecule revealed numerous important findings about its physiological and pathophysiological role. The great majority of these studies were performed on vessel segments derived from the systemic circulation but there are important observations made using cerebral vessels as well. The findings of these experimental works indicate that H2S is having a complex, pleiotropic effect on the vascular wall not only in the systemic circulation but in the cerebrovascular region as well. In this review, we summarize the most important experimental findings related to the potential role of H2S in the cerebral circulation.

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Pearce, William. "Hypoxic regulation of the fetal cerebral circulation." Journal of Applied Physiology 100, no. 2 (February 2006): 731–38. http://dx.doi.org/10.1152/japplphysiol.00990.2005.

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Fetal cerebrovascular responses to acute hypoxia are fundamentally different from those observed in the adult cerebral circulation. The magnitude of hypoxic vasodilatation in the fetal brain increases with postnatal age although fetal cerebrovascular responses to acute hypoxia can be complicated by age-dependent depressions of blood pressure and ventilation. Acute hypoxia promotes adenosine release, which depresses fetal cerebral oxygen consumption through action of adenosine on neuronal A1 receptors and vasodilatation through activation of A2 receptors on cerebral arteries. The vascular effect of adenosine can account for approximately half the vasodilatation observed in response to hypoxia. Hypoxia-induced release of nitric oxide and opioids can account for much of the adenosine-independent cerebral vasodilatation observed in response to hypoxia in the fetus. Direct effects of hypoxia on cerebral arteries account for the remaining fraction, although the vascular endothelium contributes relatively little to hypoxic vasodilatation in the immature cerebral circulation. In contrast to acute hypoxia, fetal cerebral blood flow tends to normalize during acclimatization to chronic hypoxia even though cardiac output is depressed. However, uncompensated chronic hypoxia in the fetus can produce significant changes in brain structure and function, alteration of respiratory drive and fluid balance, and increased incidence of intracranial hemorrhage and periventricular leukomalacia. At the level of the fetal cerebral arteries, chronic hypoxia increases protein content and depresses norepinephrine release, contractility, and receptor densities associated with contraction but also attenuates endothelial vasodilator capacity and decreases the ability of ATP-sensitive and calcium-sensitive potassium channels to promote vasorelaxation. Overall, fetal cerebrovascular adaptations to chronic hypoxia appear prioritized to conserve energy while preserving basic contractility. Many gaps remain in our understanding of how the effects of acute and chronic hypoxia are mediated in fetal cerebral arteries, but studies of adult cerebral arteries have produced many powerful pharmacological and molecular tools that are simply awaiting application in studies of fetal cerebral artery responses to hypoxia.

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