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Urea transporter UT-A1 and aquaporin-2 proteins decrease in response to angiotensin II or norepinephrine-induced
Janet D Klein1, Brian P Murrell, Suzanne Tucker
1Emory Univ. School of Medicine, Renal Division, 1639 Pierce Drive, NE, WMB Rm. 3319B, Atlanta, GA 30322, USA. janet.klein@emory.edu
American Journal of Physiology. Renal Physiology
|June 22, 2006
Summary
Acute hypertension from ANG II or norepinephrine decreases kidney transporters like UT-A1, AQP2, and NKCC2/BSC1. These transporter changes may cause increased sodium and water excretion during hypertension.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Molecular Biology
Background:
- The kidney's response to angiotensin II (ANG II) during malignant hypertension involves increased sodium and water excretion.
- Kidney medullary transporters play a crucial role in regulating body fluid balance.
Purpose of the Study:
- To investigate the contribution of kidney medullary transporters to the natriuretic and diuretic response during acute hypertension induced by ANG II.
- To determine if hypertension-induced transporter changes are mediated by ANG II, aldosterone, or direct effects of elevated blood pressure.
Main Methods:
- Rats were subjected to acute hypertension using ANG II infusion.
- Kidney inner medullary and outer medullary tissues were analyzed for transporter protein abundance (UT-A1, AQP2, NKCC2/BSC1).
- Comparative studies involved norepinephrine infusion (to mimic hypertension) and ANG II with spironolactone (to block aldosterone).
Main Results:
- ANG II infusion significantly decreased the abundance of UT-A1 urea transporter, AQP2 water channel, and NKCC2/BSC1 cotransporter in the kidney medulla.
- Norepinephrine-induced hypertension mimicked these transporter changes.
- ANG II's effects on transporters were observed independently of aldosterone levels.
- Water diuresis affected AQP2 and NKCC2/BSC1 but not UT-A1.
Conclusions:
- Decreased abundance of UT-A1, AQP2, and NKCC2/BSC1 proteins in the kidney medulla contributes to the diuresis and natriuresis observed during acute ANG II or norepinephrine-induced hypertension.
- These transporter alterations are likely a direct response to hypertension or ANG II, rather than being mediated by aldosterone or increased thirst.
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