Endothelial nitric oxide synthase plays an essential role in regulation of renal oxygen consumption by NO

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Abstract
Nitric oxide (NO) regulates renal O2consumption, but the source of NO mediating this effect is unclear. We explored the effects of renal NO production on O2consumption using renal cortex from mice deficient (−/−) in endothelial (e) nitric oxide synthase (NOS). O2consumption 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 O2consumption was higher in eNOS(−/−) mice than in heterozygous controls (919 ± 46 vs. 1,211 ± 133 nmol O2· min−1· g−1; P < 0.05). BK and Ram decreased O2consumption significantly less in eNOS(−/−) mice [eNOS(−/−): BK −19.0 ± 2.8%, Ram −20.5 ± 3.3% at 10−4M; control: BK −29.5 ± 2.5%, Ram −34 ± 1.6% at 10−4M]. The NO synthesis inhibitor nitro-l-arginine methyl ester (l-NAME) attenuated this decrease in control but not eNOS(−/−) mice. An NO donor inhibited O2consumption 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 O2consumption in mouse kidney.