In which of the following conditions would the patient most likely be normotensive?

Bater syndrome is a mineralocoicoid 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 conveed into bradykinin, a potent vasodilator. Because of this sequence of events, patients with Bater syndrome do not develop hypeension, even in the presence of the excess aldosterone and angiotensin II, because their hypeensive 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. Ref - Harrison's principles of internal medicine 20e pg 294, 306, 2096, 2938