Salt sensitivity of blood pressure (BP) refers to the BP responses for changes in dietary salt intake to produce meaningful BP increases or decreases. It is an independent prognostic factor in essential hypertension. Epidemiologic data demonstrates the role of high dietary salt intake in mediating cardiovascular and renal morbidity and mortality.

Salt sensitivity of BP and excess salt intake play important roles in the genesis of the cardiorenal connection. Salt sensitivity and circadian rhythm of BP are the keys to understanding the connections between cardiovascular and renal complications.

When salt intake is excessive in patients with salt-sensitive hypertension, the defect in sodium excretory capability becomes evident, resulting in elevated BP during the night. This nocturnal hypertension compensates for diminished natriuresis during the daytime and enhances pressure natriuresis during the night. Nocturnal hypertension and the non-dipper pattern of circadian BP rhythm cause cardiovascular events. When excess salt intake is loaded in patients who are in a salt-sensitive state, glomerular capillary pressure is also elevated, resulting in glomerular sclerosis and eventual renal failure. Thus, salt sensitivity and excess salt intake contribute to both cardiovascular and renal damage at the same time.

Researchers have also suggested a strong relationship between increased salt sensitivity and insulin resistance leading to metabolic syndrome and cardiovascular disease (CVD). This relationship may be predominantly responsible for epidemic of CVD in the southern Asian Indian population. This may be especially relevant to India where approximately 60% of the world’s cases of CVD reside and the salt consumption is among the highest in any large population. Apart from this, salt sensitivity has also been attributed to end-organ damage; increased risk for the development of left ventricular hypertrophy and proteinuria.

While salt restriction is definitely beneficial, recent observation suggests that treatment with the specific angiotensin receptor blocker (ARB), Azilsartan may improve salt sensitivity by selectively reducing renal proximal tubule Na+/H+ exchange. Recent studies in hypertensive patients demonstrated that Azilsartan treatment brought about a significant and persistent reduction in BP for 24 hours than other ARBs. It also changed the non-dipper pattern of BP (nocturnal hypertension) into a dipper pattern more effectively than candesartan. These findings suggested that Azilsartan could improve the circadian rhythm of BP; hence, Azilsartan could be the preferred choice in salt-sensitive hypertension.