AbstractPurpose of review
Impairment of the pressure natriuresis relationship is a central event in the pathogenesis of hypertension. Renal tubulointerstitial inflammation results in salt-sensitive hypertension and, until recently, the changes in pressure natriuresis induced by renal inflammation received little attention.Recent findings
Oxidative stress and increased intrarenal angiotensin II activity, in association with rarefaction and loss of peritubular vascular network, may be involved in the inflammation-induced blunting of the natriuresis resulting from increments in renal perfusion pressure.Summary
Here, we review the mechanisms for the impairment in pressure natriuresis resulting from renal tubulointerstitial inflammation in reference to the normal physiologic mechanisms involved in this response.