Current Therapeutic Strategies to Mitigate the eNOS Dysfunction in Ischaemic Stroke

Srivastava, Kirtiman; Bath, Philip M.W.; Bayraktutan, Ulvi

doi:10.1007/s10571-011-9777-z

Cited by 49 publications

(38 citation statements)

References 199 publications

(159 reference statements)

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“…Impairment of eNOS activity is also implicated in many cellular mechanisms of neuronal injury (Srivastava et al, 2012) and is seen after SAH, TBI and ischaemic stroke. Innate eNOS activity determines susceptibility to injury, with possession of isoforms with greater activity conferring protection against secondary neuronal insult.…”

Section: Enos Functionmentioning

confidence: 99%

The role of the nitric oxide pathway in brain injury and its treatment — From bench to bedside

Garry

Ezra

Rowland

et al. 2015

Experimental Neurology

328

221

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Nitric oxide (NO) is a key signalling molecule in the regulation of cerebral blood flow. This review summarises current evidence regarding the role of NO in the regulation of cerebral blood flow at rest, under physiological conditions, and after brain injury, focusing on subarachnoid haemorrhage, traumatic brain injury, and ischaemic stroke and following cardiac arrest. We also review the role of NO in the response to hypoxic insult in the developing brain. NO depletion in ischaemic brain tissue plays a pivotal role in the development of subsequent morbidity and mortality through microcirculatory disturbance and disordered blood flow regulation. NO derived from endothelial nitric oxide synthase (eNOS) appears to have neuroprotective properties. However NO derived from inducible nitric oxide synthase (iNOS) may have neurotoxic effects. Cerebral NO donor agents, for example sodium nitrite, appear to replicate the effects of eNOS derived NO, and therefore have neuroprotective properties. This is true in both the adult and immature brain. We conclude that these agents should be further investigated as targeted pharmacotherapy to protect against secondary brain injury.

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Section: Enos Functionmentioning

confidence: 99%

The role of the nitric oxide pathway in brain injury and its treatment — From bench to bedside

Garry

Ezra

Rowland

et al. 2015

Experimental Neurology

328

221

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“…Deficiency of eNOS contributed to increased stroke size [76]; endothelial dysfunction could be attributable to the eNOS dysfunction [77]. Increased collagen levels in SHRs were attenuated, the contents of angiotensin II (Ang II), endothelin-1 (ET-1) in the plasma, and endothelin receptor A (ETAR) in the myocardium and the ascending aorta decreased, but the level of NO and eNOS expression increased after EA stimulation at the DU20 and ST36 group in SHRs once every other day for a period of 8 weeks [61].…”

Section: The Potential Of Acupuncture For Secondary Prevention Of Strmentioning

confidence: 99%

Regulation of Hypertension for Secondary Prevention of Stroke: The Possible ‘Bridging Function' of Acupuncture

Zheng¹,

Han²,

Du³

et al. 2018

Complement Med Res

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Worldwide, stroke is the leading cause of mortality and disability, with hypertension being an independent risk factor for a secondary stroke. Acupuncture for the treatment of hypertension gains more attention in alternative and complementary medicine, but the results are inconsistent. Few studies regarding the secondary prevention of stroke by managing hypertension with acupuncture have been carried out as there are some problems regarding the antihypertensive drug status in the secondary prevention of stroke. Still, the potential of acupuncture in regulating the blood pressure for secondary stroke prevention deserves our focus. This review is based on papers recorded in the PubMed, Embase, and Web of Science databases, from their inception until March 28, 2017, and retrieved with the following search terms: hypertension and acupuncture, limited in spontaneously hypertensive rats (SHRs), stress-induced (or cold-induced) hypertensive or pre-hypertensive models. We find that, in these hypertensive animals, acupuncture could mainly influence factors related to the nervous system, oxidative stress, the endocrine system, cardiovascular function, and hemorheology, which are closely associated with the stroke outcome. This trend may give us a hint that acupuncture might well participate in the secondary prevention of stroke through these pathways when used in the management of hypertension.

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“…Although regionally selective (thalamic nuclei, prefrontal, anterior cingulate, temporal, and occipital cortices) cerebral hypoperfusion abnormalities in MDD have traditionally been attributed to depressed mood states and reduced neuronal activity [87-91][208], these findings may also be related to eNOS uncoupling [65,113,114,218] (Figure 2). Sustained cerebral hypoperfusion can impair endothelial mitochondrial oxidative function, resulting in increased synthesis of endothelial ROS [219-222].…”

Section: Introductionmentioning

confidence: 99%

Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence

Najjar¹,

Pearlman

Devinsky³

et al. 2013

J Neuroinflammation

199

174

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About one-third of people with major depressive disorder (MDD) fail at least two antidepressant drug trials at 1 year. Together with clinical and experimental evidence indicating that the pathophysiology of MDD is multifactorial, this observation underscores the importance of elucidating mechanisms beyond monoaminergic dysregulation that can contribute to the genesis and persistence of MDD. Oxidative stress and neuroinflammation are mechanistically linked to the presence of neurovascular dysfunction with blood-brain barrier (BBB) hyperpermeability in selected neurological disorders, such as stroke, epilepsy, multiple sclerosis, traumatic brain injury, and Alzheimer’s disease. In contrast to other major psychiatric disorders, MDD is frequently comorbid with such neurological disorders and constitutes an independent risk factor for morbidity and mortality in disorders characterized by vascular endothelial dysfunction (cardiovascular disease and diabetes mellitus). Oxidative stress and neuroinflammation are implicated in the neurobiology of MDD. More recent evidence links neurovascular dysfunction with BBB hyperpermeability to MDD without neurological comorbidity. We review this emerging literature and present a theoretical integration between these abnormalities to those involving oxidative stress and neuroinflammation in MDD. We discuss our hypothesis that alterations in endothelial nitric oxide levels and endothelial nitric oxide synthase uncoupling are central mechanistic links in this regard. Understanding the contribution of neurovascular dysfunction with BBB hyperpermeability to the pathophysiology of MDD may help to identify novel therapeutic and preventative approaches.

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Current Therapeutic Strategies to Mitigate the eNOS Dysfunction in Ischaemic Stroke

Cited by 49 publications

References 199 publications

The role of the nitric oxide pathway in brain injury and its treatment — From bench to bedside

The role of the nitric oxide pathway in brain injury and its treatment — From bench to bedside

Regulation of Hypertension for Secondary Prevention of Stroke: The Possible ‘Bridging Function' of Acupuncture

Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence

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