A central role for the kidney, among the systems contributing to BP regulation and the development of hypertension, has been proposed. A complex interaction between neuroendocrine factors and the kidney may underlie the propensity for such patients to retain salt and develop salt-dependent hypertension. Different individuals have different susceptibilities to the BP-raising effects of salt. The BP sensitivity to salt is defined as the inter-individual difference in the BP response to changes in dietary sodium chloride intake.

Renal excretory function is impaired in patients with salt-sensitive hypertension and results in an elevated BP. There are several studies that have provided some important evidence for the nature of inherited functional defects in renal sodium handling that cause a salt-induced increase in BP, most often associated with major alterations in the rate of renal tubular sodium chloride reabsorption. There are several factors that modulate renal function for urinary sodium excretion - the sympathetic nervous system (SNS), the renin-angiotensin system (RAS) and aldosterone and insulin. Activation of RAS increases tubular sodium reabsorption and leads to BP elevation. Apart from the classic actions of the circulating RAS, an independently functioning RAS within the kidney is thought to play a key role in regulating renal sodium excretory functions and BP.

RAS blockers; however, have been considered unsuitable for treating salt-sensitive hypertension because salt loading in hypertensive patients erases the antihypertensive effects of RAS blockers, suggesting that RAS blockers may even enhance salt sensitivity. Although negative effects of RAS blockers on salt sensitivity have been reported, the new strong ARB, azilsartan, seems to react differently to salt-sensitive hypertension.

Recent studies in hypertensive patients demonstrated that azilsartan treatment brought about a more 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.