Abstract
Salt-sensitive hypertension is closely related with natriuretic capacity of the kidney. Besides several genome-wide research reported candidate gene or gene polymorphism responsible for salt-sensitive hypertension, recently, several new factors for acquired salt-sensitive hypertension are reported. Among them, we have identified that rac1, a small GTPase, activates mineralocorticoid receptor in aldosterone-independent fashion and induces salt-sensitive hypertension in several rodent model. On the other hand, sympathoactivation in the brain and/or kidney regulate sodium handlings in the kidney. Recently it is reported that oxidative stress in the brain or in the kidney may modulate sympathetic tone. Moreover, we reported that β2 adrenoceptor alters histone acetylation and further regulates sodium resorption at distal tubules via activating glucocorticoid receptor. These regulations are to be confirmed in humans and the future, and may open a new door for diagnosis and treatment of salt-sensitive hypertension or moreover preventing development of salt-sensitive hypertension.
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