Table 1.

Antineoplastic treatments that have been associated with hypertension, common examples, and potential mechanisms for the development of hypertension

Therapeutic Class	Examples	Potential Mechanism Leading to Hypertension
VEGF Inhibitors	Bevacizumab Lenvatinib Pazopanib Ramucirumab Sorafenib Vandetanib	Glomerular injury, microvascular rarefaction, increased vascular stiffness, decreased NO production, increased endothelin-1 activation, aberrations of the RAAS system
BRAF Inhibitors	Encorafenib Vemurafenib Dabrafenib	Aberrations of the RAAS system, decreased NO production
MEK Inhibitors	Trametinib	Aberrations of the RAAS system, decreased NO production
BTK Inhibitors	Acalabrutinib Ibrutinib	Vascular tissue fibrosis, decreased NO production
Androgen Deprivation Therapy	Abiraterone	Increased synthesis of mineralocorticoid precursors
Anthracyclines / Anthracenedione	Doxorubicin Daunorubicin Epirubicin Idarubicin Mitoxantrone	Reduced capillary density, impaired neovascularization, tunica intima hyperplasia, luminal stenosis, smooth-muscle-cell dysfunction, decreased NO production
Alkylating agent	Ifosfamide	Increased risk of renal dysfunction
Platinum Based Chemotherapy	Carboplatin Cisplatin	Renal toxicity and chronic endothelial cell activation
Anti-microtubule Agents (Taxanes)	Paclitaxel	May alter sympathetic control of blood pressure
Anti-microtubule Agents (Vinka Alkaloids)	Vinblastine Vincristine	Mitosis mediated inhibition of endothelial cell proliferation
Antimetabolites	Gemcitabine	Thrombotic microangiopathy and nephrotoxicity
Radiation therapy	Abdominal radiation Head and neck radiation	Renal artery stenosis (rare) Disturbances of the baroreflex