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Am J Physiol Renal Physiol (April 10, 2002). doi:10.1152/ajprenal.00259.2001
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Articles in PresS, published online ahead of print April 10, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00259.2001
Submitted on August 17, 2001
Accepted on March 29, 2002

Effects of AT1A receptor deletion on blood pressure and sodium excretion during altered dietary salt intake

Amy J Mangrum1*, R. Ariel Gomez2, and Victoria F Norwood2

1 Department of Internal Medicine, University of Virginia, Charlottesville, VA, USA
2 Department of Pediatrics, University of Virginia, Charlottesville, VA, USA

* To whom correspondence should be addressed. E-mail: ajm7p{at}virginia.edu.

The present study was performed to investigate the role of AT1A receptors in regulating sodium balance and blood pressure maintenance during chronic dietary sodium variations in AT1A receptor (AT1A) deficient (-/-) mice. Groups of AT1A (-/-) and wild-type mice were placed on a low (LS), normal (NS) or high sodium (HS) diet for 3 weeks. AT1A (-/-) mice on LS diet had high urinary volume and low blood pressure despite increased renin and aldosterone levels. On HS, (-/-) mice demonstrated significant diuresis yet increased blood pressure to levels greater than control littermates. There was no effect of dietary sodium intake on systolic blood pressures in wild-type animals. The pressure natriuresis relationship in AT1A (-/-) mice demonstrated a shift to the left and decreased slope compared to wild-type littermates. These studies demonstrate that mice lacking the AT1A receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes.




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