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• W2045011815 abstract "Extracellular fluid volume is highly regulated, at least in part, by peripheral resistance and renal function. Nitric oxide (NO) produced by NO synthase type 3 (NOS 3) in the nonrenal vasculature may promote fluid retention by reducing systemic vascular resistance and arterial pressure. In contrast, NO produced by renal NOS 3 promotes water excretion by reducing renal vascular resistance, increasing glomerular filtration, and inhibiting reabsorption along the nephron. Thus, the net effect of NO from NOS 3 on urinary volume (UV) is unclear. We hypothesized that NO produced by NOS 3 promotes water excretion primarily due to renal tubular effects. We gave conscious wild-type and NOS 3 −/− mice an acute volume load and measured UV, blood pressure, plasma renin concentration (PRC), Na + , vasopressin, and urinary Na + and creatinine concentrations. To give the acute volume load, we trained mice to drink a large volume of water while in metabolic cages. On the day of the experiment, water was replaced with 1% sucrose, and mice had access to it for 1 h. Volume intake was similar in both groups. Over 3 h, wild-type mice excreted 62 ± 10% of the volume load, but NOS 3 −/− excreted only 42 ± 5% ( P < 0.05). Blood pressure in NOS 3 −/− was 118 ± 3 compared with 110 ± 2 mmHg in wild-type mice ( P < 0.05), but it did not change following volume load in either strain. PRC, vasopressin, and glomerular filtration rate were similar between groups. Urinary Na + excretion was 49.3 ± 7.0 in wild-type vs. 37.8 ± 6.4 μmol/3 h in NOS 3 −/− mice ( P < 0.05). Bumetanide administration eliminated the difference in volume excretion between wild-type and NOS 3 −/− mice. We conclude that 1) NO produced by NOS 3 promotes water and Na + excretion and 2) the renal epithelial actions of NO produced by NOS 3 supersede the systemic and renal vascular actions." @default.
• W2045011815 created "2016-06-24" @default.
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• W2045011815 date "2010-04-01" @default.
• W2045011815 modified "2023-09-27" @default.
• W2045011815 title "Nitric oxide produced by endothelial nitric oxide synthase promotes diuresis" @default.
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• W2045011815 doi "https://doi.org/10.1152/ajpregu.00181.2009" @default.
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