Despite significant advances in pharmacotherapy in the last several decades, control and management of hypertension and associated cardiovascular disease pathophysiology remains a challenge in 30-40% of hypertensive patients. These drug resistant patients present chronic neural overactivity and neurogenic derivation of hypertension. Thus, we believe that innovative concepts must be considered in an attempt to develop therapeutic strategies for the treatment of these neurogenic hypertensive patients. We have proposed a novel concept that a dysregulated neural-peripheral communication between the brain and bone marrow (BM) could be a key in neurogenic hypertension and its associated vascular pathophysiology. Our hypothesis suggests that vascular health is maintained by integrated signals from the autonomic brain regions to the BM which upholds a balance between angiogenic vascular reparative cells and inflammatory cells. An altered neural-BM communication as a result of an increased sympathetic drive in hypertension causes decreases in vascular reparative cells and increases inflammatory cells. This shift in balance would not only provoke inflammation-induced vascular damage, but also compromise its repairability. Evidence will be presented in support of this hypothesis.