Pathophysiology of salt-sensitive hypertension: a new scope of an old problem

Abstract

It has been recognized for many years that salt intake is one of the main environmental factors responsible for the development of hypertension. More than 30 years ago, Guyton and co-workers postulated a relationship between blood pressure and natriuresis which maintains sodium balance and extracellular volume; thus an impaired ability of the kidney to excrete sodium requires an increase in blood pressure to increase natriuresis and correct the sodium balance, resulting in hypertension. Currently, the mechanisms responsible for the alterations mentioned above remain under investigation. Among them, microvascular and tubulointerstitial injury induce salt retention and development of salt-sensitive hypertension that appears to be mediated in part by lymphocytes and macrophages infiltrating the tubulointerstitium that produce angiotensin II and stimulate oxidative stress. In the post-angiotensin salt-sensitive hypertension model, angiotensin levels are elevated despite systemic angiotensin II levels being suppressed, and the local angiotensin II levels correlate with the presence of intrarenal inflammation and cortical vasoconstriction. Under these conditions, blockade of the angiotensin II AT1 receptors ameliorate cortical vasoconstriction. Thus, the renal angiotensin system in association with interstitial immune infiltrating cells may play a pivotal role in the development and maintenance of salt-sensitive hypertension.