<s>[INST] context: Bartter syndrome is a mineralocorticoid excess state caused by a defect in chloride reabsorption in the kidneys. The defect in chloride reabsorption in the ascending tubule also affects the reabsorption of so­dium; therefore, there is an augmented distal delivery of sodium with increased exchange of sodium for po­tassium and hydrogen ions in the distal tubule, produc­ing a hypokalemic metabolic alkalosis. Hypokalemia is a stimulus of renin release from the juxtaglomerular (JG) apparatus, which results in JG apparatus hyper­plasia. Activation of the renin-angiotensin-aldoste­rone system increases the production of angiotensin II and aldosterone. Hypokalemia also increases the synthesis of prostaglandin E2 and 12 in the kidneys. Both of these chemical mediators are potent vasodila­tors. Angiotensin II and aldosterone stimulate the syn­thesis of renal kallikrein, which is then converted into bradykinin, a potent vasodilator. Because of this se­quence of events, patients with Bartter syndrome do not develop hypertension, even in the presence of the excess aldosterone and angiotensin II, because their hypertensive effects are offset by the vasodilatation induced by the prostaglandins and bradykinin. In ad­dition, for unexplained reasons, these patients are resis­tant to the effects of infused angiotensin II. [/INST] question: In which of the following conditions would the (patient most likely be normotensive? | options: A: Primary hyperparathyroidism B: Hypothyroidism C: Cushing syndrome D: Barter syndrome | answer: D </s>