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Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112-2699
This study was
performed to determine the influence of neuronal nitric oxide synthase
(nNOS) on renal arteriolar tone under conditions of normal,
interrupted, and increased volume delivery to the macula densa segment
and on the microvascular responses to angiotensin II (ANG II).
Experiments were performed in vitro on afferent (21.2 ± 0.2 µm)
and efferent (18.5 ± 0.2 µm) arterioles of kidneys harvested from
male Sprague-Dawley rats, using the blood-perfused juxtamedullary
nephron technique. Superfusion with the specific nNOS inhibitor,
S-methyl-L-thiocitrulline
(L-SMTC), decreased afferent and
efferent arteriolar diameters, and these decreases in arteriolar
diameters were prevented by interruption of distal volume delivery by
papillectomy. When 10 mM acetazolamide was added to the blood perfusate
to increase volume delivery to the macula densa segment, afferent
arteriolar vasoconstrictor responses to
L-SMTC were enhanced, but this
effect was again completely prevented after papillectomy. In contrast,
the arteriolar diameter responses to the nonselective NOS inhibitor,
N
-nitro-L-arginine
(L-NNA) were only
attenuated by papillectomy. L-SMTC (10 µM) enhanced the
efferent arteriolar vasoconstrictor response to ANG II but did not
alter the afferent arteriolar vasoconstrictor responsiveness to ANG II.
In contrast, L-NNA (100 µM)
enhanced both afferent and efferent arteriolar vasoconstrictor
responses to ANG II. These results indicate that the modulating
influence of nNOS on afferent arteriolar tone of juxtamedullary
nephrons is dependent on distal tubular fluid flow. Furthermore, nNOS
exerts a differential modulatory action on the juxtamedullary
microvasculature by enhancing efferent, but not afferent, arteriolar
responsiveness to ANG II.
renal microcirculation; autoregulation; N
-nitro-L-arginine; S-methyl-L-thiocitrulline; angiotensin II
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