Key result
Endothelial nitric oxide synthase deficiency in mice resulted in higher basal renal oxygen consumption compared to controls (1,211 vs 919 nmol O2/min/g; P<0.05) and attenuated responses to bradykinin.
Absolute Event Rate: 1211% vs 919%
p-value: p=<0.05
Endothelial nitric oxide synthase (eNOS) is the primary source of nitric oxide responsible for regulating renal oxygen consumption in the mouse kidney.
eNOS mediates NO suppression of renal O2 consumption in vitro; leaves open its physiologic role in vivo.
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 O(2). min(-1). g(-1); 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 10(-4) M; control: BK -29.5 +/- 2.5%, Ram -34 +/- 1.6% at 10(-4) 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.
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Adler et al. (2001) studied this question. eNOS deficiency vs. Heterozygous controls was evaluated on Basal O2 consumption (nmol O2/min/g) (p=<0.05). Endothelial nitric oxide synthase deficiency in mice resulted in higher basal renal oxygen consumption compared to controls (1,211 vs 919 nmol O2/min/g; P<0.05) and attenuated responses to bradykinin.
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