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Division of Nephrology, Departments of 1 Medicine and 2 Physiology, New York Medical College, Valhalla, New York 10595
Nitric oxide (NO) regulates
renal O2 consumption, but the source of NO mediating this
effect is unclear. We explored the effects of renal NO production on
O2 consumption using renal cortex from mice deficient
(
/) in endothelial (e) nitric oxide synthase (NOS). O2
consumption was determined polarographically in slices of cortex from
control and eNOS(/) mice. NO production was stimulated by
bradykinin (BK) or ramiprilat (Ram) in the presence or absence of an
NOS inhibitor. Basal O2 consumption was higher in
eNOS(/) mice than in heterozygous controls (919 ± 46 vs.
1,211 ± 133 nmol O2 · min
1 · g1;
P < 0.05). BK and Ram decreased O2
consumption significantly less in eNOS(/) mice [eNOS(/): BK
19.0 ± 2.8%, Ram 20.5 ± 3.3% at 104 M;
control: BK 29.5 ± 2.5%, Ram 34 ± 1.6% at
104 M]. The NO synthesis inhibitor
nitro-L-arginine methyl ester (L-NAME)
attenuated this decrease in control but not eNOS(/) mice. An NO
donor inhibited O2 consumption similarly in both groups independent of the presence of L-NAME. These results
demonstrate that NO production by eNOS is responsible for regulation of
renal O2 consumption in mouse kidney.
bradykinin; renal physiology; ramiprilat; nitric oxide
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