A class of drugs designed to inhibit cancer growth could have a dual application as blood pressure monitors, according to research out of Georgetown University.

Oncology professor Anton Wellstein, MD, PhD, and colleagues found that a medication used by oncologists to inhibit fibroblast growth factors (FGFs) could not only stall the spread of certain cancers, but keep hypertension in control, as well. FGFs increase blood vessel size to accommodate cancer growth, Wellstein and co-authors wrote in a Hypertension-published study, so cancer patients are given FGF inhibitors to restrict room for cancer cells to multiply and inhibit angiogenesis.

FGFs have a systemic effect on blood pressure, according to Wellstein et al.’s paper, suggesting the same inhibitors used in cancer patients could be applied to hypertensive individuals to regulate blood pressure and control hypertension-linked illnesses.

“We work on angiogenesis mechanisms as they relate to cancer,” Wellstein told Cardiovascular Business of his work. “I have known that targeting angiogenesis, for example by blocking VEGF signaling with an antibody or a small molecule inhibitor, will cause hypertension. Thus, there is a direct connection between mechanisms that control blood vessel growth and survival and their control of blood flow, which will impact blood pressure.”

Wellstein and his team had gathered this knowledge from previous research, and for this trial focused on an FGF-regulating protein known as FGFBP1, which is produced by FGF binding protein 1. The researchers found that a population in Eastern Europe had previously been identified as hypertensive carriers of the FGFBP1 gene, which led to over-expression of FGFBP1 in these patients’ kidney tissues—the major control hubs for blood pressure.

In this study, Wellstein and colleagues tested the effects of FGFBP1 in mice models, since the protein can be easily switched on or off in the rodents. When turned on, the protein nudged the mice’s blood pressure up by 30 mm Hg—a sizeable jump from regular levels to worrisome hypertension.

“The strong hypertensive effect seen when initiating FGF pathway activation was surprising,” Wellstein said.

The scientists found that hypertension regulation by FGFBP1 occurred in resistance vessels, which control blood flow to various tissues. FGFBP1 increased vessel response to angiotensin II, which subsequently constricted blood vessels and made blood pressure rise. In mice given an FGF inhibitor, Wellstein and co-authors found decreased sensitivity to angiotensin II and, therefore, lower blood pressure.

Wellstein said his team is now working on understanding if receptor selective inhibitors of the FGF pathway have differential effects or not, but he knows this is a step forward for cardiovascular medicine.

“That we may take advantage of drugs developed to treat cancer by modulating FGF signaling may be useful in the treatment of cardiovascular disease,” he said. “This does apply for the FGF pathway and will be very interesting to pursue and find out what particular branches are more and less efficacious and adverse event-prone.”