Trial reportHypertension (Dallas, Tex. : 1979)2011
Contrary effects of the receptor tyrosine kinase inhibitor vandetanib on constitutive and flow-stimulated nitric oxide elaboration in humans.
Trial report in Hypertension (Dallas, Tex. : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 55 citations in OpenAlex.
- Ebselen does not improve oxidative stress and vascular function in patients with diabetes: a randomized, crossover trial.American journal of physiology. Heart and circulatory physiology · 2016Trial
- The effect of salsalate therapy on endothelial function in a broad range of subjects.Journal of the American Heart Association · 2014Trial
- VEGF inhibitor-induced proteinuria: the role of hypertension and vascular endothelial dysfunction.Journal of pharmaceutical health care and sciences · 2026Review
- Feasibility study protocol for the evaluation of home blood pressure in patients receiving angiogenesis inhibitor therapy: a multicenter observational study.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Observational
- Vascular Toxicities of Cancer Therapies: 2025 Update.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Cardiovascular Safety of VIAN-c4551, an Antiangiogenic Peptide Derived From Vasoinhibin.Drug development research · 2025Article
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- Acute vascular and cardiac effects of lenvatinib in mice.Cardio-oncology (London, England) · 2025Article
- Hypertension toxicity of VEGFR-TKIs in cancer treatment: incidence, mechanisms, and management strategies.Archives of toxicology · 2025Review
- Cancer Therapy and Exercise Intolerance: The Heart Is But a Part:JACC. CardioOncology · 2024Review
- Vascularised cardiac spheroids-on-a-chip for testing the toxicity of therapeutics.Scientific reports · 2024Article
- Cardiotoxicity Induced by Protein Kinase Inhibitors in Patients with Cancer.International journal of molecular sciences · 2022Review
- Hypertension Induced by Combination Therapy of Cancer: A Systematic Review and Meta-Analysis of Global Clinical Trials.Frontiers in pharmacology · 2021Review
- Changes in blood pressure during treatment with the tyrosine kinase inhibitor lenvatinib.Clinical kidney journal · 2021Article
- Vascular toxicities with VEGF inhibitor therapies-focus on hypertension and arterial thrombotic events.Journal of the American Society of Hypertension : JASH · 2018Review
- Mechanisms of VEGF (Vascular Endothelial Growth Factor) Inhibitor-Associated Hypertension and Vascular Disease.Hypertension (Dallas, Tex. : 1979) · 2018Review
- Cardio-Oncology: mechanisms of cardiovascular toxicity.F1000Research · 2018Review
- Hypertension in cancer patients treated with anti-angiogenic based regimens.Cardio-oncology (London, England) · 2015Review
- In vitro pharmacological profiling of R406 identifies molecular targets underlying the clinical effects of fostamatinib.Pharmacology research & perspectives · 2015Article
- The contribution of VEGF signalling to fostamatinib-induced blood pressure elevation.British journal of pharmacology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Vascular endothelial growth factor regulates neoplastic angiogenesis through production of endothelium-derived NO. We performed a prospective evaluation of vascular function during treatment with vandetanib, a vascular endothelial growth receptor 2 and 3 receptor tyrosine kinase inhibitor, to determine the effects of vascular endothelial growth receptor signal interruption on endothelial function in humans. Seventeen patients with stage IV breast cancer received dose-escalated vandetanib in combination with low-dose oral chemotherapy. We measured blood pressure, systemic nitrate/nitrite levels, and brachial artery vascular function. In vitro analyses of cultured endothelial cells were performed to determine the effect of vandetanib on NO production, akt(473) phosphorylation, and endothelial NO synthase protein content and membrane localization. Vandetanib treatment for 6 weeks significantly increased blood pressure, decreased resting brachial artery diameter, and decreased plasma systemic nitrate/nitrite levels compared with baseline. Flow-mediated vasodilation was preserved, and no change was noted in nitroglycerin-mediated vasodilation. In vitro, endothelial cell nitrite levels and akt(473) phosphorylation were reduced and vascular endothelial growth receptor 2 levels did not change, but endothelial NO synthase membrane concentration doubled. Vandetanib reduces constitutive NO production and increases blood pressure, yet flow-stimulated NO bioavailability was preserved. Changes in vascular function with tyrosine kinase inhibition are complex and require further study in humans.
Indexed as
Identifiers
What OpenQuestion holds
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.