Does angiotensin II cross the blood–brain barrier?

Roncevic, Dusan

doi:10.1038/hr.2012.55

Cited by 8 publications

(6 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ANGII in the brain may have originated from peripherally infused ANGII which enter the brain parenchyma via impaired BBB which was damaged by sustained hypertension induced by itself 39,40 . Also, it is reported that systematically infused ANGII can cross BBB at a very low degree through the AT1R mediated transcytosis of BBB endothelial cells 41 . The newly synthesized ANGII in Brain RAS 42 also can contribute to depressive-like behavior.…”

Section: Discussionmentioning

confidence: 99%

Chronically infused angiotensin II induces depressive-like behavior via microglia activation

Park

You

Yang

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Brain inflammation is one of hypotheses explaining complex pathomechanisms of depression. Angiotensin II (ANGII), which is associated with hypertension, also induces brain inflammation. However, there is no animal study showing the direct relationship between ANGII and depression. To address this issue, ANGII-containing osmotic pumps were implanted into adult male C57BL/6 mice subcutaneously for subacute (7 days) and chronic (at least 21 days) periods and behavioral and molecular analyses were conducted. Chronic infusion of ANGII into mice induced depressive-like behaviors, including the tail suspension test and forced swimming test, which were reversed by imipramine. Chronic infusion of ANGII also induced microglial activation in the hippocampus with increase of Il-1β mRNA and decrease of Arg1 mRNA. In addition, chronic ANGII infusion activated the hypothalamic–pituitary–adrenal axis (HPA axis) and resulted in decreased hippocampal glucocorticoid receptor level. However, subacute ANGII infusion did not induce significant molecular and behavioral changes in mice compared to that of control. The molecular and behavioral changes by chronic ANGII infusion were reversed by co-treatment of minocycline or telmisartan. In addition, ANGII treatment also induced the pro-inflammatory changes in BV-2 microglial cells. Our results indicate that ANGII can induce depressive-like behaviors via microglial activation in the hippocampus and HPA axis hyperactivation in mice. These might suggest possible mechanism on depressive symptom in chronic hypertensive state.

show abstract

Section: Discussionmentioning

confidence: 99%

Chronically infused angiotensin II induces depressive-like behavior via microglia activation

Park

You

Yang

et al. 2020

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Angiotensin II (ATII) regulates blood pressure. It is produced by the peripherally but able to cross the BBB [ 175 ] where it can also target the brain vasculature.…”

Section: Candidate Central and Peripheral Factors Inducing Proliferatmentioning

confidence: 99%

How the Body Talks to the Brain; Peripheral Mediators of Physical Activity-Induced Proliferation in the Adult Hippocampus

Bolijn

Lucassen

2015

BPL

View full text Add to dashboard Cite

In the hippocampal dentate gyrus, stem cells maintain the capacity to produce new neurons into adulthood. These adult-generated neurons become fully functional and are incorporated into the existing hippocampal circuit. The process of adult neurogenesis contributes to hippocampal functioning and is influenced by various environmental, hormonal and disease-related factors.One of the most potent stimuli of neurogenesis is physical activity (PA). While the bodily and peripheral changes of PA are well known, e.g. in relation to diet or cardiovascular conditions, little is known about which of these also exert central effects on the brain. Here, we discuss PA-induced changes in peripheral mediators that can modify hippocampal proliferation, and address changes with age, sex or PA duration/intensity. Of the many peripheral factors known to be triggered by PA, serotonin, FGF-2, IGF-1, VEGF, β-endorphin and adiponectin are best known for their stimulatory effects on hippocampal proliferation. Interestingly, while age negatively affects hippocampal proliferation per se, also the PA-induced response to most of these peripheral mediators is reduced and particularly the response to IGF-1 and NPY strongly declines with age. Sex differences per se have generally little effects on PA-induced neurogenesis. Compared to short term exercise, long term PA may negatively affect proliferation, due to a parallel decline in FGF-2 and the β-endorphin receptor, and an activation of the stress system particularly during conditions of prolonged exercise but this depends on other variables as well and remains a matter of discussion. Taken together, of many possible mediators, serotonin, FGF-2, IGF-1, VEGF, β-endorphin and adiponectin are the ones that most strongly contribute to the central effects of PA on the hippocampus. For a subgroup of these factors, brain sensitivity and responsivity is reduced with age.

show abstract

“…; Yarlagadda et al . ; Roncevic, ). However, several studies suggest that Ang‐II and cytokines gain access to the brain via the CVOs (John & Buckingham, ; Shi et al .…”

Section: Introductionmentioning

confidence: 99%

Neuroinflammation in heart failure: new insights for an old disease

Díaz

Toledo

Andrade

et al. 2019

The Journal of Physiology

View full text Add to dashboard Cite

Heart failure (HF) is a complex clinical syndrome affecting roughly 26 million people worldwide. Increased sympathetic drive is a hallmark of HF and is associated with disease progression and higher mortality risk. Several mechanisms contribute to enhanced sympathetic activity in HF, but these pathways are still incompletely understood. Previous work suggests that inflammation and activation of the renin-angiotensin system (RAS) increases sympathetic drive. Importantly, chronic inflammation in several brain regions is commonly observed in aged populations, and a growing body of evidence suggests neuroinflammation plays a crucial role in HF. In animal models of HF, central inhibition of RAS and pro-inflammatory cytokines normalizes Hugo S. Díaz H. S. Díaz and others J Physiol 598.1 sympathetic drive and improves cardiac function. The precise molecular and cellular mechanisms that lead to neuroinflammation and its effect on HF progression remain undetermined. This review summarizes the most recent advances in the field of neuroinflammation and autonomic control in HF. In addition, it focuses on cellular and molecular mediators of neuroinflammation in HF and in particular on brain regions involved in sympathetic control. Finally, we will comment on what is known about neuroinflammation in the context of preserved vs. reduced ejection fraction HF. Abstract figure legendIntegrative physiology of heart failure progression: Heart failure (HF) is characterized by chronic inflammation, renin-angiotensin system (RAS) overactivity, sympathoexcitation and cardiac dysfunction. Sympathoexcitation and RAS activation occur early in HF progression as a compensatory response to haemodynamic challenges. Chronic activation of these compensatory mechanisms becomes maladaptive and has toxic effects on cardiac muscle leading to electrophysiological abnormalities and initiation of fibrotic processes. RAS activation also enhances chemoreflex sensitivity (further exacerbating sympathetic activation) and promotes diffuse inflammation. Both systemic and brain RAS and inflammation feed back to exacerbate sympathoexcitation, generating a vicious cycle that contributes to further cardiac dysfunction.

show abstract

Does angiotensin II cross the blood–brain barrier?

Cited by 8 publications

References 5 publications

Chronically infused angiotensin II induces depressive-like behavior via microglia activation

Chronically infused angiotensin II induces depressive-like behavior via microglia activation

How the Body Talks to the Brain; Peripheral Mediators of Physical Activity-Induced Proliferation in the Adult Hippocampus

Neuroinflammation in heart failure: new insights for an old disease

Contact Info

Product

Resources

About