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Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575
Experiments were performed to test the
hypothesis that the impact of endogenous nitric oxide (NO) on ANG
II-induced renal arteriolar constriction is reduced in rats with
insulin-dependent diabetes mellitus (65 mg/kg streptozotocin; STZ).
Arteriolar diameter responses to exogenous ANG II were quantified
before and during NO synthase inhibition (100 µM
N
-nitro-L-arginine;
L-NNA) by using the in vitro blood-perfused juxtamedullary
nephron technique. Afferent arteriolar lumen diameter averaged 20.7 ± 2.0 µm in Sham kidneys and 25.9 ± 1.3 µm in STZ kidneys
(P < 0.05). Efferent arteriolar diameter did not differ between Sham and STZ rats. In kidneys from Sham rats, afferent and
efferent arteriolar responses to ANG II (0.1-10.0 nM) were exaggerated significantly by L-NNA. L-NNA also
augmented efferent arteriolar ANG II responses in kidneys from STZ rats
(high-glucose bath) but did not alter ANG II responses in afferent
arterioles from STZ rats. L-NNA also accentuated efferent,
but not afferent, arteriolar ANG II responses in STZ kidneys during
acute restoration of bath glucose to normal levels. Superoxide
dismutase (150 U/ml) restored the ability of L-NNA to allow
exaggerated afferent arteriolar responses to ANG II in kidneys from STZ
rats. These observations indicate that superoxide anion suppresses the
modulatory influence of endogenous NO on ANG II-induced afferent
arteriolar constriction in diabetes mellitus.
efferent arteriole; N-nitro-L-arginine; rat; streptozotocin; superoxide dismutase
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