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Articles in PresS, published online ahead of print November 12, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00340.2002
Submitted on September 20, 2002
Accepted on November 11, 2002
1 Department of Physiology, Tulane University Health Sciences Center, New Orleans, LA, USA
2 Department of Medicine, Duke University and Durham Veterans Affair Medical Centers, Durham, NC, USA
* To whom correspondence should be addressed. E-mail: lharris{at}tulane.edu.
The relative contributions of AT1A and AT1B receptors on afferent arteriole autoregulatory capability and afferent and efferent arteriole responses to angiotensin (Ang) II are not known. Experiments were conducted in kidneys from Wild-type (WT) and AT1A-/- mice utilizing the in vitro blood perfused juxtamedullary nephron technique. Direct measurements of afferent (AAD) and efferent arteriolar diameters (EAD) were assessed at a renal artery pressure (RAP) of 100mmHg. AAD averaged 14.8±0.8µm in WT and 14.9±0.8µm in AT1A-/- mice. AAD significantly decreased by 7±1, 16±1, and 26±2% in WT mice and by 11±1, 20±2, and 30±3% in AT1A-/- mice (120, 140, 160 mmHg). AAD autoregulatory capability was not affected by the absence of AT1A receptors. AAD responses to 10nM AngII were significantly blunted in AT1A-/- mice compared to WT (-22±2 vs -37±5%). AngII (0.1 to 10nM) failed to elicit any change in EAD in AT1A-/- mice. AAD and EAD reductions to AngII were blocked by 1µM Candesartan. We conclude that afferent arteriole vasoconstrictor responses to AngII are mediated by AT1A and AT1B receptors, while efferent arteriole vasoconstrictor responses to AngII are mediated by only AT1A receptors in the mouse kidney.
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