ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Treatment for cerebral small vessel disease: effect of relaxin on the function and structure of cerebral parenchymal arterioles during hypertension.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Emerging biomarkers and frontier therapies: unveiling the role of endothelial dysfunction in cerebral small vessel disease.Frontiers in neurology · 2025Review
- Altered Cerebral Blood Flow and Potential Neuroprotective Effect of Human Relaxin-2 (Serelaxin) During Hypoxia or Severe Hypovolemia in a Sheep Model.International journal of molecular sciences · 2020Article
- Relaxin reduces endothelium-derived vasoconstriction in hypertension: Revealing new therapeutic insights.British journal of pharmacology · 2020Article
- Isoflurane-Induced Postoperative Neurovascular and Cognitive Dysfunction Is Associated with VEGF Overexpression in Aged Rats.Journal of molecular neuroscience : MN · 2019Article
- Potential therapeutic use of relaxin in accelerating closure of cranial bone defects in mice.Physiological reports · 2019Article
- Augmented astrocyte microdomain CaGlia · 2019Article
- Transient receptor potential vanilloid-4 channels are involved in diminished myogenic tone in brain parenchymal arterioles in response to chronic hypoperfusion in mice.Acta physiologica (Oxford, England) · 2019Article
- The importance of comorbidities in ischemic stroke: Impact of hypertension on the cerebral circulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- Targeting the Relaxin Pathway for Liver Disease Treatment.European medical journal. Hepatology · 2018Article
- The relaxin peptide family - potential future hope for neuroprotective therapy? A short review.Neural regeneration research · 2018Review
- Relaxin as a Therapeutic Target for the Cardiovascular Complications of Diabetes.Frontiers in pharmacology · 2018Review
- Vascular actions of relaxin: nitric oxide and beyond.British journal of pharmacology · 2017Review
- Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke.Circulation research · 2017Review
- Novel Anti-fibrotic Therapies.Frontiers in pharmacology · 2017Review
- Microvascular Dysfunction and Cognitive Impairment.Cellular and molecular neurobiology · 2016Review
- Enhanced serelaxin signalling in co-cultures of human primary endothelial and smooth muscle cells.British journal of pharmacology · 2016Article
- Regulation of myogenic tone and structure of parenchymal arterioles by hypertension and the mineralocorticoid receptor.American journal of physiology. Heart and circulatory physiology · 2015Article
- Astrocyte contributions to flow/pressure-evoked parenchymal arteriole vasoconstriction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Relaxin activates peroxisome proliferator-activated receptor γ (PPARγ) through a pathway involving PPARγ coactivator 1α (PGC1α).The Journal of biological chemistry · 2015Article
- Increased pressure-induced tone in rat parenchymal arterioles vs. middle cerebral arteries: role of ion channels and calcium sensitivity.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We investigated the effect of hypertension on the function and structure of cerebral parenchymal arterioles (PAs), a major target of cerebral small vessel disease (SVD), and determined whether relaxin is a treatment for SVD during hypertension. PAs were isolated from 18-wk-old female normotensive Wistar-Kyoto (WKY) rats, spontaneous hypertensive rats (SHRs), and SHRs treated with human relaxin 2 for 14 d (4 μg/h; n=8/group) and studied using a pressurized arteriograph system. Hypertension reduced PA inner diameter (58±3 vs. 49±3 μm at 60 mmHg in WKY rats, P<0.05), suggesting inward remodeling that was reversed by relaxin (56±4 μm, P<0.05). Relaxin also increased PA distensibility in SHRs (34±2 vs. 10±2% in SHRs, P<0.05). Relaxin was detected in cerebrospinal fluid (110±30 pg/ml) after systemic administration, suggesting that it crosses the blood-brain barrier (BBB). Relaxin receptors (RXFP1/2) were not detected in cerebral vasculature, but relaxin increased vascular endothelial growth factor (VEGF) and matrix metalloproteinase 2 (MMP-2) expression in brain cortex. Inhibition of VEGF receptor tyrosine kinase (axitinib, 4 mg/kg/d, 14 d) had no effect on increased distensibility with relaxin, but caused outward hypertrophic remodeling of PAs from SHRs. These results suggest that relaxin crosses the BBB and activates MMP-2 in brain cortex, which may interact with PAs to increase distensibility. VEGF appears to be involved in remodeling of PAs, but not relaxin-induced increased distensibility.
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