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Purpose Gitelman’s syndrome (GS) presents normo-hypotension and absence of cardiovascular–renal remodeling despite high angiotensin II (Ang II), activation of renin–angiotensin–aldosterone system and is a human model of endogenous antagonism of Ang II signaling, opposite to hypertension. GS’s clinical presentation leads to questions regarding what features might be responsible. One area of investigation...
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