{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T23:39:17Z","timestamp":1782257957430,"version":"3.54.5"},"reference-count":31,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,5,1]]},"abstract":"<jats:p>Nitric oxide (NO) regulates renal O<jats:sub>2<\/jats:sub>consumption, but the source of NO mediating this effect is unclear. We explored the effects of renal NO production on O<jats:sub>2<\/jats:sub>consumption using renal cortex from mice deficient (\u2212\/\u2212) in endothelial (e) nitric oxide synthase (NOS). O<jats:sub>2<\/jats:sub>consumption was determined polarographically in slices of cortex from control and eNOS(\u2212\/\u2212) mice. NO production was stimulated by bradykinin (BK) or ramiprilat (Ram) in the presence or absence of an NOS inhibitor. Basal O<jats:sub>2<\/jats:sub>consumption was higher in eNOS(\u2212\/\u2212) mice than in heterozygous controls (919 \u00b1 46 vs. 1,211 \u00b1 133 nmol O<jats:sub>2<\/jats:sub>\u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 g<jats:sup>\u22121<\/jats:sup>; P &lt; 0.05). BK and Ram decreased O<jats:sub>2<\/jats:sub>consumption significantly less in eNOS(\u2212\/\u2212) mice [eNOS(\u2212\/\u2212): BK \u221219.0 \u00b1 2.8%, Ram \u221220.5 \u00b1 3.3% at 10<jats:sup>\u22124<\/jats:sup>M; control: BK \u221229.5 \u00b1 2.5%, Ram \u221234 \u00b1 1.6% at 10<jats:sup>\u22124<\/jats:sup>M]. The NO synthesis inhibitor nitro-l-arginine methyl ester (l-NAME) attenuated this decrease in control but not eNOS(\u2212\/\u2212) mice. An NO donor inhibited O<jats:sub>2<\/jats:sub>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 O<jats:sub>2<\/jats:sub>consumption in mouse kidney.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.5.f838","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:16:58Z","timestamp":1514038618000},"page":"F838-F843","source":"Crossref","is-referenced-by-count":40,"title":["Endothelial nitric oxide synthase plays an essential role in regulation of renal oxygen consumption by NO"],"prefix":"10.1152","volume":"280","author":[{"given":"Stephen","family":"Adler","sequence":"first","affiliation":[{"name":"Division of Nephrology, Departments of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harer","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Departments of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kit 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