The development of salt-sensitive hypertension regulated by PSGL-1 gene in mice

Our results indicate that PSGL-1 is involved in the development of salt-sensitive hypertension via vascular inflammation and injury. The high salt induced inflammation may be initiated by leukocytes and endothelial cells adhesion through PSGL-1 binding with P-selectin or/and E-selectin.

Chronic inflammatory is involved in the development of salt-sensitive hypertension and other cardiovascular diseases. PSGL-1 plays an important role in the inflammatory response.

In this study, we used PSGL-1-/- and PSGL-1+/+ mice fed with high salt diet to measure the blood pressure, inflammatory response and vascular injury. We found that, in PSGL-1+/+ mice, high salt diet resulted in high blood pressure with the increased expression of serum inflammatory cytokines IL-6, IL-1β and TNFɑ, vascular injury markers MCP-1, ET-1, and VWF, and renal macrophages and T cells infiltration, and endothelium-dependent acetylcholine vasodilation dysfunction. However, the influence was not found in PSGL-1-/- mice. The deficiency of PSGL-1 prevented the increased adhesion of peripheral blood mononuclear cells to endothelial cells by high salt environment. Conclusions: Our results indicate that PSGL-1 is involved in the development of salt-sensitive hypertension via vascular inflammation and injury. The high salt induced inflammation may be initiated by leukocytes and endothelial cells adhesion through PSGL-1 binding with P-selectin or/and E-selectin.