Abstract
PURPOSE OF REVIEW: Rapidly emerging evidence implicates an important role of gut-brain-bone marrow (BM) axis involving gut microbiota (GM), gut epithelial wall permeability, increased production of pro-inflammatory BM cells and neuroinflammation in hypertension (HTN). However, the precise sequence of events involving these organs remains to be established. Furthermore, whether an impaired gut-brain-BM axis is a cause or consequence of HTN is actively under investigation. This will be extremely important for translation of this fundamental knowledge to novel, innovative approaches for the control and management of HTN. Therefore, our objectives are to summarize the latest hypothesis, provide evidence for and against the impaired gut, BM and brain interactions in HTN and discuss perspectives and future directions. RECENT FINDINGS: Hypertensive stimuli activate autonomic neural pathways resulting in increased sympathetic and decreased parasympathetic cardiovascular modulation. This directly affects the functions of cardiovascular-relevant organs to increase blood pressure. Increases in sympathetic drive to the gut and BM also trigger sequences of signaling events that ultimately contribute to altered GM, increased gut permeability, enhanced gut- and brain-targeted pro-inflammatory cells from the BM in perpetuation and establishment of HTN. SUMMARY: In this review, we present the mechanisms involving the brain, gut, and BM, whose dysfunctional interactions may be critical in persistent neuroinflammation and key in the development and establishment of HTN.