Is neurogenic hypertension related to vascular inflammation of the brainstem?

Essential hypertension is idiopathic although it is accepted as a complex polygenic trait with underlying genetic components, which remain unknown. Our supposition is that hypertension involves activation of the sympathetic nervous system. One pivotal region controlling arterial pressure set point is nucleus tractus solitarii (NTS). We recently identified that pro-inflammatory molecules, such as junctional adhesion molecule-1 (JAM-1), were over expressed in endothelial cells of the microvasculature supplying the NTS in an animal model of human hypertension (the spontaneously hypertensive rat) compared to normotensive Wistar-Kyoto rats (WKY). Over expression of JAM-1 in NTS of WKY rats was pro-hypertensive and induced leukocyte adherence to the microvasculature. Since leukocyte adhesion causes cytokine release, we found expression of monocyte chemoattractant protein-1 (MCP-1) was higher in the NTS of SHR while inter-leukin-6 (IL-6) was lower compared to the WKY rat. Inflammation of the brainstem microvasculature may increase vascular resistance within the brainstem. High brainstem vascular resistance and its inflammation may release pathological paracrine signaling molecules affecting central neural cardiovascular activity conducive to neurogenic hypertension.