Our analysis validates loci containing genes with prior physiological connection to BP such as BDNF, FAM208A, and CACNA2D252–54. The neurotrophin Brain Derived Neurotrophic Factor (BDNF) modulates angiotensin 11 in the brain to elevate BP in experimental models; higher serum levels correlate with reduced risk of cardiovascular disease and mortality52. In experimental models FAM208A, which is thought to be a transcription factor, is a strong candidate for a QTL for BP54. The gene CACNA2D2 encodes a subunit of the L-type calcium channel that is most abundantly expressed in the atrium and in neurones and may be a target for negatively chronotropic and inotropic calcium channel antagonists which reduce BP55.
