Analyses of molecular mechanism of hypertensive cardio-renal relationships focusing on post-transcriptional regulations of ion-transporters.

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Our research revealed the genetic and biological significance of molecules involved in "Molecular pathogenesis of tubular mechanisms leading to salt-sensitive hypertension." Renal tubular epithelial cells, joined by tight junction with each other, were highly differentiated, forming a tubule lumen of the ureteric bud-derived embryologically. Our research to date, a renal tubular RA system, the ENaC working in aldosterone-sensitive distal tubule cell work as endogenous endocrine systems for maintaining homeostatis. We have established molecular pathogenesis models maintaining homeostasis by regulating sodium reabsorption and via its collapse leading to pathology of salt-sensitivity, developing hypertension.