The relationship between cancer and high blood pressure (hypertension) is rarely a simple direct cause-and-effect link. The connection is complex and often indirect, involving specialized tumors, the side effects of modern treatments, and shared underlying health factors. Understanding this intricate relationship is an emerging focus in medicine, particularly in cardio-oncology. While cancer can influence blood pressure through hormonal disruption, elevated pressure is more commonly caused by necessary medical interventions and the body’s systemic response to malignancy.
Cancers That Directly Affect Blood Pressure Regulation
A few rare cancers directly cause high blood pressure by interfering with the body’s hormonal system. These malignancies typically arise from the adrenal glands, which produce hormones that regulate blood pressure. The tumor mass acts as an overactive endocrine factory, leading to secondary hypertension.
A primary example is a pheochromocytoma, a tumor of the adrenal medulla that releases excessive catecholamines (like norepinephrine and epinephrine) into the bloodstream. These potent hormones cause widespread constriction of blood vessels and increased heart rate, resulting in significantly elevated blood pressure that may be sustained or occur in severe, episodic spikes. Another instance is an aldosterone-producing adrenocortical carcinoma, which secretes too much aldosterone. This hormone causes the kidneys to retain salt and water, increasing blood volume and blood pressure.
Treatment-Induced Hypertension
The most frequent scenario where cancer and hypertension intersect is when the treatment itself causes blood pressure to rise. Modern targeted therapies, while effective at fighting cancer, can disrupt the mechanisms that keep blood vessels healthy and pliable. This side effect, known as cancer therapy-induced hypertension, is a growing concern for oncologists and cardiologists alike.
VEGF Inhibitors
A major class of drugs implicated are Vascular Endothelial Growth Factor (VEGF) inhibitors, used to starve tumors by blocking the formation of new blood vessels. VEGF is also essential for maintaining the health of normal blood vessels, particularly the endothelium. By inhibiting this pathway, these drugs reduce the production of nitric oxide (NO), a molecule that causes blood vessels to relax. The resulting imbalance favors vasoconstriction, which increases resistance to blood flow and drives up blood pressure.
Other Treatments
This process can also lead to microvascular rarefaction—a reduction in the density of small blood vessels—which increases overall resistance in the circulatory system. Certain proteasome inhibitors, used to treat multiple myeloma, also cause hypertension, possibly by disrupting nitric oxide regulation. Furthermore, conventional chemotherapies, such as platinum-based compounds like cisplatin, can cause chronic endothelial injury and damage the kidneys over time. This long-term damage includes nephrotoxicity and reduced NO availability, contributing to later-onset hypertension.
Radiation Therapy
Radiation therapy to the abdomen or pelvis can also lead to hypertension by damaging the kidneys or their supplying arteries. This damage can cause radiation nephropathy, impairing the kidney’s ability to regulate blood pressure and fluid balance. Radiation can also cause the arteries to narrow (renal artery stenosis), which activates the body’s blood pressure-raising system to compensate for reduced blood flow.
Shared Risk Factors and Systemic Inflammation
Cancer and hypertension share a significant overlap in underlying risk factors and biological pathways. Both conditions are common in the aging population and are often linked by lifestyle factors such as obesity, physical inactivity, and smoking. Individuals with pre-existing conditions like diabetes or chronic kidney disease are already at a higher risk for both, establishing a correlation that is not causal.
The presence of a tumor can also induce chronic systemic inflammation. This persistent, low-grade inflammation involves the release of chemical messengers that stress the cardiovascular system. This inflammatory state contributes to endothelial dysfunction, making blood vessels less responsive and potentially worsening hypertension. The biological mechanisms driving both diseases are intertwined, involving processes like oxidative stress.
Monitoring Blood Pressure During Oncology Care
Active monitoring and management are essential components of oncology care, given the high probability of developing or worsening hypertension during treatment. Patients starting therapies known to increase blood pressure, especially VEGF inhibitors, should monitor their pressure at home daily or weekly during the first few cycles. This proactive approach allows for the early detection of elevated pressures before they cause significant cardiovascular damage or necessitate an interruption of the cancer regimen.
Lifestyle modifications play a supporting role, including maintaining a healthy weight, engaging in regular physical activity, and reducing sodium intake. When medication is necessary, Angiotensin-Converting Enzyme (ACE) inhibitors or Angiotensin Receptor Blockers (ARBs) are often the first-line choice, as they may offer protective benefits to the heart. For complex cases, patients are often referred to a cardio-oncology specialist, who focuses on the intersection of heart disease and cancer treatment. The goal is to keep blood pressure optimally controlled to minimize cardiovascular risk and ensure the patient can safely continue their cancer therapy.