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Central Cardiovascular Circuits Contribute to the Neurovascular Dysfunction in Angiotensin II Hypertension
Open accessAbstract
Hypertension, a powerful risk factor for stroke and dementia, has damaging effects on the brain and its vessels. In particular, hypertension alters vital cerebrovascular control mechanisms linking neural activity to cerebral perfusion. In experimental models of slow-developing hypertension, free radical signaling in the subfornical organ (SFO), one of the forebrain circumventricular organs, is critical for the hormonal release and sympathetic activation driving the elevation in arterial pressure. However, the contribution of this central mechanism to the cerebrovascular alterations induced by hypertension remains uncertain. We tested the hypothesis that free radical production in the SFO is involved in the alterations in cerebrovascular regulation produced by hypertension. In a mouse model of gradual hypertension induced by chronic administration of subpressor doses of angiotensin II (AngII), suppression of free radicals in the SFO by overexpression of CuZn-superoxide dismutase (CuZnSOD) prevented the alteration in neurovascular coupling and endothelium-dependent responses in somatosensory cortex induced by hypertension. The SFO mediates the dysfunction via two signaling pathways. One involves SFO-dependent activation of the paraventricular hypothalamic nucleus, elevations in plasma vasopressin, upregulation of endothelin-1 in cerebral resistance arterioles and activation of endothelin type A receptors. The other pathway depends on activation of cerebrovascular AngII type 1 (AT1) receptors by AngII. Both pathways mediate vasomotor dysfunction by inducing vascular oxidative stress. The findings implicate for the first time the SFO and its efferent hypothalamic pathways in the cerebrovascular alterations induced by AngII, and identify vasopressin and endothelin-1 as potential therapeutic targets to counteract the devastating effects of hypertension on the brain.
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“Thus, in humans as in animal models, hypertension disrupts all the major factors regulating the cerebral circulation, including neurovascular coupling and endothelial vasomotor function (10,11).”
From Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension (2016) · cites this paper as [10]
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“The cerebrovascular dysfunction is mediated by activation of ANGII type 1 receptors (AT1Rs) and vascular oxidative stress produced by a NOX2-containing NADPH oxidase (10,15).”
From Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension (2016) · cites this paper as [10]
In the citing paper
“Administration of low doses of ANGII for 2 weeks, which results in a slow-developing rise in BP (“slow pressor” hypertension) (14), induces profound alterations in neurovascular coupling and endothelium-dependent vasodilation (10,15).”
From Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension (2016) · cites this paper as [10]
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“As illustrated in Figure 7B, ANGII induces an increase in ROS signal, assessed by hydroethidine microfluorography (10,35) in PVMs.”
From Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension (2016) · cites this paper as [10]
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Metadata
- Authors
- Capone, C., Faraco, G., Peterson, J. R., Coleman, C., Anrather, J., Milner, T. A., Pickel, V. M., Davisson, R. L., & Iadecola, C.
- Affiliations
- Weill Cornell Medicine (US)
- Rockefeller University (US)
- Cornell University (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-04-04
- Volume
- 32
- Issue
- 14
- Pages
- 4878-4886
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3328774
- OpenAlex
- W2132051579
- Cited by
- 106
- References
- 67
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 7 · 2023: 2 · 2022: 10 · 2021: 4 · 2020: 8 · 2019: 10 · 2018: 8 · 2017: 8 · 2016: 5 · 2015: 11 · 2014: 5 · 2013: 13 · 2012: 2
- FWCI
- 6.38
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL-96571, R01HL063887, HL98351, P01HL096571, R01HL098351)
- National Institute of Neurological Disorders and Stroke (R01NS073666)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- subfornical organ, neurovascular coupling, cerebrovascular dysfunction, oxidative stress, Cu/Zn superoxide dismutase, paraventricular nucleus, vasopressin, endothelin-1, ETA receptor, angiotensin II type 1 receptor, somatosensory cortex, circumventricular organs, stroke risk
- MeSH terms
- Angiotensin II, Animals, Cerebrovascular Circulation, Endothelium, Vascular, Hypertension, Male, Mice, Inbred C57BL, Subfornical Organ, Reactive Oxygen Species, Gene Transfer Techniques, Receptor, Angiotensin, Type 1, Mice
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