The kidney responds to high levels of angiotensin II (Ang II), as may occur during malignant hypertension, by increasing sodium and water excretion. To study whether kidney medullary transporters contribute to this response, rats were made hypertensive using Ang II. Within 3 days of giving Ang II, systolic blood pressure (BP) was increased (200 mmHg), vs control (130 mmHg), and remained high through day 14. Kidney inner medullary (IM) tip and base, and outer medulla were analyzed for transporter protein abundances. There were significant decreases in: UT-A1 urea transporter; aquaporin-2 (AQP2) water channel; and NKCC2/BSC1 Na⁺-K⁺-2Cl^- cotransporter. To determine if the decreases were a response to hypertension, Ang II, or an Ang II-induced increase in aldosterone, rats were given: 1) norepinephrine (to increase BP); and 2) Ang II plus spironolactone (to block the mineralocorticoid receptor). Norepinephrine (7 days) increased BP, urine volume, sodium excretion, and decreased urine osmolality and UT-A1, AQP2, and NKCC2/BSC1 abundances, similar to Ang II. Ang II alone or with spironolactone yielded similar increases in BP, urine volume, and urine osmolality, and decreases in UT-A1 and AQP2 proteins in the IM tip. Plasma vasopressin was unaffected by treatment. Water diuresis did not change UT-A1, but decreased AQP2 and NKCC2/BSC1 abundances. We conclude that decreases in UT-A1, AQP2, and NKCC2/BSC1 proteins may contribute to the diuresis and natriuresis that occurs following Ang II or norepinephrine-induced acute hypertension, and does not appear to involve Ang II-stimulation of aldosterone or thirst.