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1 Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112; and 2 Department of Medicine, Duke University, and Durham Veterans Affairs Medical Centers, Durham, North Carolina 27705
The relative contributions of
AT1A and AT1B receptors to afferent arteriolar
autoregulatory capability and afferent and efferent arteriolar
responses to 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 arterial pressure of 100 mmHg. AAD averaged
14.8 ± 0.8 µm for WT and 14.9 ± 0.8 µm for
AT1A/ mice. AAD significantly decreased by 7 ± 1, 16 ± 1, and 26 ± 2% for WT mice and by 11 ± 1, 20 ± 2, and 30 ± 3% for AT1A/ mice (120, 140, 160 mmHg). AAD autoregulatory capability was not affected by the
absence of AT1A receptors. AAD responses to 10 nM ANG II
were significantly blunted for AT1A/ mice compared with
WT (22 ± 2 vs. 37 ± 5%). ANG II (0.1-10 nM)
failed to elicit any change in EAD for AT1A/ mice. AAD
and EAD reductions in ANG II were blocked by 1 µM candesartan. We
conclude that afferent arteriole vasoconstrictor responses to ANG II
are mediated by AT1A and AT1B receptors,
whereas efferent arteriolar vasoconstrictor responses to ANG II are
mediated by only AT1A receptors in the mouse kidney.
afferent arteriole; efferent arteriole; juxtamedullary nephron; candesartan; autoregulation
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