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Case Reports
. 2012 Sep;60(3):607-15.
doi: 10.1161/HYPERTENSIONAHA.112.196774. Epub 2012 Jul 30.

Management of antiangiogenic therapy-induced hypertension

Nilka de Jesus-Gonzalez  1 , Emily Robinson, Javid Moslehi, Benjamin D Humphreys
Affiliations
Case Reports

Management of antiangiogenic therapy-induced hypertension

Nilka de Jesus-Gonzalez et al. Hypertension. 2012 Sep.
No abstract available

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Figures

Figure 1
Figure 1
Blood pressure monitoring and therapeutic interventions in a 56 years old male patient with metastatic renal cell carcinoma treated with sunitinib who developed asymptomatic hypertension after sunitinib therapy was started.
Figure 2
Figure 2
Proposed mechanisms leading to VEGF signaling pathway inhibitor-induced hypertension. a) Activation of VEGFR-2 by VEGF-A leads to subsequent activation of multiple pathways including phosphatidylinositol-3-kinase (PI3K)-AKT. PI3K-AKT phosphorylates and activates endothelial nitric oxide synthase (eNOS), increasing NO production. NO migrates to adjacent vascular smooth muscle cells, binds soluble guanylate cyclase (sGC) leading to cGMP generation and subsequent vasodilation mediated by cGMP-dependent kinases. When VEGF signaling pathway is inhibited, NO pathway is suppressed and ET-1 pathway is stimulated, promoting vasoconstriction and subsequent hypertension. The source of ET-1 is unknown. b) VEGF maintains capillary network integrity. When VEGF signaling pathway is inhibited, rarefaction, or reduction of the density of capillary beds, may occur.
Figure 3
Figure 3
Initial cardiovascular evaluation and monitoring of blood pressure in candidates for antinagiogenic therapy. CVD, cardiovascular disease; DM, diabetes mellitus; LVH, left ventricular hypertrophy; BP, blood pressure; SCr, serum creatinine; ACR, albumin to creatinine ratio; FBG, fasting blood glucose; SBP, systolic blood pressure; DBP, diastolic blood pressure; HTN, hypertension.
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