Sodium transport in endothelial cells--a brief review

Abnormalities in endothelial cell functions play a significant role in the pathogenesis of hypertension and altherosclerosis. Ion transport, particularly sodium (Na+) transport, serves important functions in both housekeeping and stimulus-response pathways in endothelial cells. Cell cultures provide useful experimental systems to investigate the operation and the regulation of various Na+ transporters. Among these Na+ transport systems, activities of Na+ pump, Na+-K+-Cl- cotransport, and Na+-H+ exchange have all been reported in cultured endothelial cells. Similar to those in other cells, these transport systems are responsible for the establishment and maintenance of ionic composition and volume of the endothelial cell. Alterations of intracellular Na+,H+, and/or cell volume can activate individual transport pathways and usually can serve as a feedback regulatory mechanism to achieve constant cellular volume and ions. In addition, hormones and vasoactive peptides modulate the activities of these transporters; physicochemical modifications of the membrane by cholesterol enrichment or oxidant stress also affect Na+ transport. The maintenance of Na+(or K+) gradients across plasma membrane by Na+ pump are important for nutrient uptake and protein synthesis in endothelial cells. Regulatory volume increase or decrease also occur and are mediated via activation of Na(+-)K(+-)Cl-cotransporter (and Na(+-)H+ exchanger, but significance unclear) or KCl loss, respectively. Na(+-)K(+-)Cl- cotransport is also altered by vasoactive peptide and may play a role in modulating vascular properties. Oxidant stress appears to alter all 3 systems: inhibit Na(+-)K(+-)Cl- cotransport and Na(+-)H+ exchange while stimulate Na+ pump, these changes may be part of the mechano-transduction pathway in endothelial cells.