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. 2021 Apr 2;128(7):1040–1061. doi: 10.1161/CIRCRESAHA.121.318051

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© 2021 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 2. — Pathophysiological mechanisms underlying VEGF (vascular endothelial growth factor) inhibitor (VEGFI)-induced hypertension and possible therapeutic interventions. Clinically, four different major classes of agents to inhibit VEGF signaling can be distinguished: (1) monoclonal antibodies directed against circulating VEGF; (2) soluble decoy receptors (VEGF-traps), scavenging freely available VEGF; (3) monoclonal antibodies against the vascular endothelial growth factor receptor (VEGFR); (4) TKI with anti-VEGFR activity that act on the intracellular tyrosine kinase domains of VEGFR to inhibit their activation. Multiple mechanisms contribute to VEGFI-induced hypertension, including an imbalance between vasoconstrictor (ET-1 [endothelin-1]) and vasodilator factors (nitric oxide [NO]), oxidative stress, microvascular rarefaction, renal injury, and decreased lymphangiogenesis. Conventional antihypertensive drugs, including calcium channel blockers and angiotensin-converting enzyme inhibitors / angiotensin II receptor blockers can be used in the treatment of VEGFI-induced hypertension. Additional potential treatment options include salt restriction, ET-1 receptor antagonists and aspirin. However, ET-1 receptor antagonists are currently not registered for the treatment of systemic hypertension. mAb indicates monoclonal antibody; PlGF, placental growth factor; and TKI, tyrosine kinase inhibitor (Illustration credit: Ben Smith).