Salt-sensitive hypertension is produced by a decrease in salt renal excretion after a salt overload. Over the last few years, a new theory has been developed to explain this condition based on renal tissue inflammation. This process begins with free radicals production in renal tissue due to oxidative metabolism. Then they favor a renal inflammation mechanism with T-lymphocytes infiltration and other immune cells. Essentially, T-lymphocytes determine an increase in angiotensin ii production which raises sodium and water retention. Association among autoimmune diseases and hypertension may be explained, in part, by the relationship between salt-sensitive hypertension and renal inflammation. The use of antioxidant drugs and the development of new medicaments may be a choice for treating patients affected with this condition.
CITATION STYLE
Torres, Y. C., Portela, A. E. S., & Maria Garrido Bősze, I. (2014). Role of renal inflammation in the physiopathology of salt-sensitive hypertension. Archivos de Cardiologia de Mexico. Instituto Nacional de Cardiologia Ignazio Chavez. https://doi.org/10.1016/j.acmx.2014.02.002
Mendeley helps you to discover research relevant for your work.