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

Nitric oxide (NO) regulates renal O-2 consumption, but the source of NO med iating this effect is unclear. We explored the effects of renal NO producti on on O-2 consumption using renal cortex from mice deficient (-/-) in endot helial (e) nitric oxide synthase (NOS). O-2 consumption was determined pola rographically in slices of cortex from control and eNOS(-/-) mice. NO produ ction was stimulated by bradykinin (BK) or ramiprilat (Ram) in the presence or absence of an NOS inhibitor. Basal O-2 consumption was higher in eNOS(- /-) mice than in heterozygous controls (919 +/- 46 vs. 1,211 =/- 133 nmol O -2.min(-1).g(-1); P< 0.05). BK and Ram decreased O2 consumption significant ly less in eNOS( -/-) mice [eNOS(-/-): BK -19.0 +/- 2.8%, Ram -20.5 +/- 3.3 % at 10(-4) M; control: BK -29.5 +/- 2.5%, Ram -34 +/- 1.6% at 10(-4) M]. T he NO synthesis inhibitor nitro-L-arginine methyl ester (L-NAME) attenuated this decrease in control but not eNOS( -/-) mice. An NO donor inhibited O- 2 consumption similarly in both groups independent of the presence of L-NAM E. These results demonstrate that NO production by eNOS is responsible for regulation of renal O-2 consumption in mouse kidney.