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Renal function in the AT1A receptor knockout mouse during normal and volume-expanded conditions
L Cervenka1, K D Mitchell, M I Oliverio
1Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana, USA.
Kidney International
|November 26, 1999
Summary
Mice lacking the angiotensin II (Ang II) AT1A receptor maintained normal kidney function but had lower blood pressure. Volume expansion normalized blood pressure and Ang II levels, indicating fluid volume
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Endocrinology
Background:
- The role of angiotensin II (Ang II) AT1A receptors in renal regulation is complex.
- Understanding Ang II's impact on renal hemodynamics and sodium balance is crucial.
Purpose of the Study:
- To investigate the function of AT1A receptors in regulating renal hemodynamics, sodium excretion, and glomerulotubular balance.
- To examine the impact of AT1A receptor deficiency on Ang II levels under normal and volume-expanded conditions.
Main Methods:
- Utilized AT1A receptor-deficient mice and wild-type controls.
- Measured aortic pressure, glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion.
- Determined plasma and kidney Ang II levels via radioimmunoassay under euvolemic and volume-expanded states.
Main Results:
- AT1A receptor-deficient mice exhibited lower mean arterial pressures (MAPs) but maintained normal GFR, RPF, and sodium excretion.
- Volume expansion increased MAP in deficient mice and normalized plasma Ang II levels.
- Glomerulotubular balance was preserved in the absence of AT1A receptors.
Conclusions:
- Absence of AT1A receptors does not impair chronic renal regulation.
- Low blood pressure in deficient mice is linked to reduced fluid volume.
- Extracellular fluid volume and blood pressure dominate short-loop feedback regulation of plasma Ang II levels.