Urea Transporter UT-A1 and Aquaporin-2 Proteins Decrease in Response to Angiotensin II or Norepinephrine-Induced Acute Hypertension
| Title: | Urea Transporter UT-A1 and Aquaporin-2 Proteins Decrease in Response to Angiotensin II or Norepinephrine-Induced Acute Hypertension |
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| Authors: | Klein, MD, PhD, Janet; Murrell, Brian P.; Tucker, Suzanne; Kim, Young-Hee; Sands, Jeff M. |
| Publisher: | American Journal of Physiology: Renal Physiology |
| Date Published: | November 01, 2006 |
| Reference Number: | 711 |
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This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
During episodes of malignant hypertension, high levels of the hormone, angiotensin II (ANG II) appear in the blood. The kidneys respond to these high ANG II levels by excreting higher levels of sodium and water than usual. Klein, et al., wanted to know if the key transport protein involved in urine concentration (the UT-A1 urea transporter, aquaporin-2 (AQP2), and the NKCC2/BSC1 Na+ -K= -2C1¯ cotransporter) decreased in number during episodes of malignant hypertension. If so, this decrease would contribute to the excessive excretion of urine (diuresis) and sodium in the urine (natriuresis) associated with the hypertension.
To test for this, the experimenters treated rats with ANG II to make them hypertensive. Within three days, all indicators pointed to hypertension and remained high through the last day of the two-week test period. From day seven through fourteen, the rats showed significant decreases in UT-A1, AQP2 and NKCC2/BSC1 Na+ -K= -2C1¯. Further experimentation confirmed that these decreases were due to hypertension, not to the increase in the hormone, aldosterone, that also occurs through exposure to ANG II. The researchers state that the decrease of these three transport proteins likely contribute to the diuresis and natriuresis experienced by the hypertensive rats.



