Review Article
Potential Therapeutic Strategies for Hypertension-Exacerbated Cardiotoxicity of Anticancer Drugs
Table 1
Comparative summary of prohypertensive effects of anticancer chemotherapeutic drugs and the adjunvants commonly used in cancer patients.
| Class of drugs | Typical drugs | Potential mechanisms for the prohypertensive effects | Representative references |
| Anthracyclines | Doxorubicin, daunorubicin, epirubicin, and idarubicin | Oxidative stress and apoptotic/fibrotic and inflammatory changes in vascular wall; endothelial dysfunction | [12–17] | VEGF inhibitors | Bevacizumab and vandetanib | Endothelial dysfunction; reduced nitric oxide bioavailability; increased endothelin production | [18, 19] | Tyrosine kinase inbibitors | Sunitinib, sorabenib, and pazopanib | Endothelial dysfunction; reduced nitric oxide bioavailability; vascular rarefaction; hypothyroidism | [20–22] | Alkylating agents | Cyclophosphamide and cisplatin | Endothelial dysfunction; arterial vasoconstriction; renal and vascular damage | [23, 24] | Glucocorticoids | Dexamethasone | Salt and fluid retention | [25, 26] | Erythropoietin | rhuEPO | Increase in erythrocyte mass and blood viscosity; direct vasopressor effect | [27–29] |
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VEGF: vascular endothelial growth factor; rhuEPO: recombinant human erythropoietin.
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