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Updated: Aug 16, 2026

In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
Effects of VEGF on hemodynamics and cardiac function: characterization and mechanisms
1Department of Cardiovascular Research, Genentech Inc, South San Francisco, CA 94080, USA.
Insights
Vascular endothelial growth factor (VEGF) aids angiogenesis but can cause adverse hemodynamic effects like hypotension and tachycardia. Strategies to mitigate these side effects are crucial for clinical applications.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Regenerative Medicine
Background:
- Vascular endothelial growth factor (VEGF) promotes angiogenesis, crucial for treating ischemic diseases.
- VEGF's clinical utility is potentially limited by adverse hemodynamic and cardiac effects.
- Understanding VEGF's impact on cardiovascular function is vital.
Purpose of the Study:
- To review the hemodynamic profile induced by VEGF.
- To elucidate the mechanisms behind VEGF-mediated hemodynamic changes.
- To discuss strategies for preventing or attenuating VEGF's side effects.
Main Methods:
- Literature review focusing on studies investigating VEGF's hemodynamic effects.
- Analysis of data on blood pressure, heart rate, cardiac output, and vascular parameters.
- Examination of the role of nitric oxide in VEGF-induced vasodilation and hyperpermeability.
Main Results:
- VEGF administration is associated with hypotension, tachycardia, and reduced cardiac output and stroke volume.
- Hemodynamic alterations are primarily mediated by VEGF-induced vasodilation and vascular hyperpermeability.
- Nitric oxide plays a key role in mediating these VEGF-induced cardiovascular effects.
Conclusions:
- VEGF's beneficial angiogenic effects are counterbalanced by significant hemodynamic challenges.
- Nitric oxide-dependent vasodilation and hyperpermeability underlie VEGF's adverse cardiovascular impact.
- Developing preventative or attenuating strategies is essential for safe VEGF-based therapies.
Abstract:
Vascular endothelial growth factor (VEGF), a mitogen specific for endothelial cells, produces beneficial angiogenesis in animal models of ischemic diseases; however, its side effects on hemodynamics and cardiac function may limit clinical use for some indications. This review focuses on the VEGF-induced hemodynamic profile, including hypotension, tachycardia, decreases in cardiac output and stroke volume, and changes in preload and afterload. The hemodynamic effects of VEGF are due to vasodilation and vascular hyperpermeability, which are mainly mediated by nitric oxide. Finally, the regimen or strategy for attenuation or prevention of these side effects is discussed.
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