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Subjects Clinical trials Prognosis. Access through your institution. Buy or subscribe. Change institution. Learn more. References Forouzanfar MH, Liu P, Roth GA, Ng M, Biryukov S, Marczak L, et al. Article Google Scholar Beaney T, Schutte AE, Stergiou GS, Borghi C, Burger D, Charchar F, et al.
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Article CAS Google Scholar Kunutsor SK, Laukkanen JA. Article CAS Google Scholar Download references. Author information Authors and Affiliations Department of Medicine, Sultan Qaboos University Hospital, Muscat, Oman Sunil K.
Nadar Department of Cardiology, Worcestershire Acute Hospitals NHS trust, Worcester, UK Deepak Goyal Authors Sunil K. Nadar View author publications. View author publications. Ethics declarations Conflict of interest The authors declare that they have no conflict of interest.
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About the journal Announcements Journal Information Open access publishing About the Editors About the Partners Contact For Advertisers Subscribe. Microglia plays an important role in the brain innate immune response.
Even though a possible modulatory effect of microglia on NVC remains to be established, activated microglia may, through the production of ROS and proinflammatory cytokines, impact NVC functions. In the model of hypertension induced by chronic administration of Ang II, increased proinflammatory cytokines expression was reported in the PVN, inducing microglial activation.
Hypertension is characterized by an imbalance between pro- and anti-inflammatory cytokines and chemokines, maintaining low-grade inflammation. Anti-hypertensive drugs have been commonly used for a few decades in order to reduce BP and the risk of cardio and cerebrovascular events.
Even though these therapies successfully lower BP in most individuals, many hypertensive patients remain at risk for cardio and cerebrovascular events, and resistance to such treatments is still observed.
This lack of effects of anti-hypertensive drugs may be due to unresolved inflammation. Some anti-hypertensive drugs, such as angiotensin-converting enzyme ACE inhibitors and AT 1 R antagonists, exert anti-inflammatory actions by inhibiting proinflammatory cascades induced by Ang II in humans , and experimental models of hypertension.
In fact, treatments with statins can reduce levels of proinflammatory cytokines, such as IL-1β, IL-6, TNF-α, ICAM-1, and CRP in patients with acute coronary syndromes.
They can also enhance mRNA and protein expression of endothelial NOS eNOS and therefore induce a protective anti-inflammatory effect through the production of NO. In the last decades, the possibility of using anti-inflammatory drugs, known for their beneficial effects on vascular functions, has been explored in order to treat hypertension.
Nonsteroidal anti-inflammatory drugs NSAIDs , such as aspirin, ibuprofen, and naproxen, have been considered as potential treatments for hypertension based on their important anti-inflammatory properties. NSAIDs not only improve endothelial function, but also inhibit NF-κB, cyclooxygenase COX -1, and COX-2, as well as the production of proinflammatory cytokines, ROS, MMPs, and prostaglandins, all of which are present in the brain.
In recent years, extensive investigations revealed specific inflammatory therapeutic targets to treat hypertension and associated end-organ damages. Anti-inflammatory IL-4, IL and proinflammatory IL-1β, IL-6 IL, IL, IL, or IL cytokines, which are tightly involved in hypertension development and related end-organ damages have started to be investigated as possible therapeutic targets.
In animal models of hypertension, inhibition of some proinflammatory cytokines, such as IL-6 and IL, has been shown to be beneficial for the cerebral vasculature. Indeed, hypertension is known to increase cerebral levels of IL-6, which was shown to affect CBF, NVC, and BBB integrity.
IL, a cytokine known to induce brain damage by acting directly on brain cells or indirectly through the disruption of BBB and neurovascular functions, is another potential target. As such, in patient suffering from psoriasis, ILA inhibition has also led to a reduction in vascular inflammation and is currently under evaluation in a prospective vascular inflammation trial Vascular Inflammation in Psoriasis-Secukinumab; NCT Consequently, knowing that all of these immunotherapeutic approaches reduce vascular inflammation or restore vascular functions, they could all be potential therapeutic options to prevent hypertension and its associated cerebrovascular risks.
Emerging evidence from preclinical studies points to a strong relationship between hypertension, altered cerebrovascular functions, neuroinflammation, and brain dysfunctions. Hypertension, through systemic inflammation, can alter the structure and function of cerebral blood vessels and therefore impair the fundamental mechanisms responsible to maintain brain homeostasis.
Indeed, oxidative stress and inflammation induced by hypertension are key contributors to neurovascular and endothelial dysfunctions. However, many questions remain unresolved. For example, which animal model would allow better translational discoveries about the immune role in cerebrovascular diseases in hypertension?
Also, are mechanical and circulating proinflammatory factors responsible for cerebrovascular impairments in hypertension, or do neurogenic factors induce hypertension in parallel of cerebrovascular impairments?
Considering the importance of the immune system in physiological functions and for protecting against pathogens, which element should be targeted to optimize beneficial effects in hypertensive patients? Even though promising results in clinical trials have shown a reduction in systemic inflammation and related vascular dysfunctions, the impact of immunotherapies on brain inflammation and associated cerebrovascular complications need a profound evaluation.
Immunomodulating drugs could be a potential therapeutic approach against hypertension-associated cerebrovascular disorders, such as stroke, vascular cognitive impairment, and AD.
Assistance with manuscript revision was provided by Diane Vallerand. Figures were created with BioRender. Hélène Girouard was supported by the Fonds de recherche du Québec—Santé FRQS; Qiu C , Winblad B , Fratiglioni L.
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Thank you for visiting nature. You are using inflajmation browser version with Hypertenaion support Herbal remedies for bronchitis CSS. To Hypertension and inflammation the best Carbohydrate awareness in food labeling, we inflammagion you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Hypertension that is considered idiopathic is called essential hypertension and accordingly has no clear culprit for its cause.
Inlfammation, the Hypertension and inflammation link between hypertension and neurodegenerative diseases Hypwrtension to be understood. Recent evidence indicates Hair growth for receding hairline inflammation is a common Hypertension and inflammation trait for Hypertensoon hypertension and neurodegenerative diseases. Low-grade chronic inflam,ation at the systemic and central nervous system levels is now recognized to contribute to the physiopathology of hypertension. This review speculates that inflammation represents a mediator between hypertension and neurodegenerative diseases, either by a decrease in cerebral blood flow or a disruption of the blood—brain barrier which will, in turn, let inflammatory cells and neurotoxic molecules enter the brain parenchyma. This may impact brain functions including cognition and contribute to neurodegenerative diseases. This review will thus discuss the relationship between hypertension, systemic inflammation, cerebrovascular functions, neuroinflammation, and brain dysfunctions.
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