ArticleHypertension (Dallas, Tex. : 1979)2013
Circulating endothelin-1 alters critical mechanisms regulating cerebral microcirculation.
Article in Hypertension (Dallas, Tex. : 1979), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
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- Endothelin-1 triggers oxidative stress and cytokine release in human microglia cells through ETRB-dependent mechanisms.Frontiers in cellular neuroscience · 2025Article
- Sepsis modulates cortical excitability and alters the local and systemic hemodynamic response to seizures.Scientific reports · 2022Article
- The Ca2+-gated channel TMEM16A amplifies capillary pericyte contraction and reduces cerebral blood flow after ischemia.The Journal of clinical investigation · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Small Vessel Disease: Ancient Description, Novel Biomarkers.International journal of molecular sciences · 2022Review
- Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021Review
- Frequency selective neuronal modulation triggers spreading depolarizations in the rat endothelin-1 model of stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Endothelial S1PCirculation research · 2021Article
- Intravascular Endothelin-1 does not trigger or increase susceptibility to Spreading Depolarizations.The journal of headache and pain · 2020Article
- Small Vessel Disease-Related Dementia: An Invalid Neurovascular Coupling?International journal of molecular sciences · 2020Review
- Exposure to Blast Overpressure Impairs Cerebral Microvascular Responses and Alters Vascular and Astrocytic Structure.Journal of neurotrauma · 2019Article
- Article
- Brain Vasculature and Cognition.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- The Role of NADPH Oxidases and Oxidative Stress in Neurodegenerative Disorders.International journal of molecular sciences · 2018Review
- Fasudil preserves lung endothelial function and reduces pulmonary vascular remodeling in a rat model of end‑stage pulmonary hypertension with left heart disease.International journal of molecular medicine · 2018Article
- Changes in Cerebral Arteries and Parenchymal Arterioles With Aging: Role of Rho Kinase 2 and Impact of Genetic Background.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response.Nature neuroscience · 2018Article
- Oxidative Stress: A Major Player in Cerebrovascular Alterations Associated to Neurodegenerative Events.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Endothelin-1 (ET1) is a potent vasoconstrictor peptide implicated in the cerebrovascular alterations occurring in stroke, subarachnoid hemorrhage, and brain trauma. Brain or circulating levels of ET1 are elevated in these conditions and in risk factors for cerebrovascular diseases. Most studies on the cerebrovascular effects of ET1 have focused on vascular smooth muscle constriction, and little is known about the effect of the peptide on cerebrovascular regulation. We tested the hypothesis that ET1 increases cerebrovascular risk by disrupting critical mechanisms regulating cerebral blood flow. Male C57Bl6/J mice equipped with a cranial window were infused intravenously with vehicle or ET1, and somatosensory cortex blood flow was assessed by laser Doppler flowmetry. ET1 infusion increased mean arterial pressure and attenuated the blood flow increase produced by neural activity (whisker stimulation) or neocortical application of the endothelium-dependent vasodilator acetylcholine but not A23187. The cerebrovascular effects of ET1 were abrogated by the ET(A) receptor antagonist BQ123 and were not related to vascular oxidative stress. Rather, the dysfunction was dependent on Rho-associated protein kinase activity. Furthermore, in vitro studies demonstrated that ET1 suppresses endothelial nitric oxide (NO) production, assessed by its metabolite nitrite, an effect associated with Rho-associated protein kinase-dependent changes in the phosphorylation state of endothelial NO synthase. Collectively, these novel observations demonstrate that increased ET1 plasma levels alter key regulatory mechanisms of the cerebral circulation by modulating endothelial NO synthase phosphorylation and NO production through Rho-associated protein kinase. The ET1-induced cerebrovascular dysfunction may increase cerebrovascular risk by lowering cerebrovascular reserves and increasing the vulnerability of the brain to cerebral ischemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.