Nitric oxide produced by endothelial nitric oxide synthase promotes diuresis
| العنوان: | Nitric oxide produced by endothelial nitric oxide synthase promotes diuresis |
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| المؤلفون: | Kamal M. Kassem, Marcela Herrera, William H. Beierwaltes, Jeffrey L. Garvin, Jazmin M. Pérez-Rojas |
| المصدر: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 298:R1050-R1055 |
| بيانات النشر: | American Physiological Society, 2010. |
| سنة النشر: | 2010 |
| مصطلحات موضوعية: | medicine.medical_specialty, Nitric Oxide Synthase Type III, Endothelium, Physiology, Diuresis, Blood Pressure, Nitric Oxide, Nitric oxide, Mice, chemistry.chemical_compound, Heart Rate, Physiology (medical), Internal medicine, Renin, Renin–angiotensin system, Extracellular fluid, medicine, Animals, Diuretics, Bumetanide, Mice, Knockout, biology, Reabsorption, Sodium, Articles, Mice, Inbred C57BL, Nitric oxide synthase, Endocrinology, medicine.anatomical_structure, chemistry, Creatinine, biology.protein |
| الوصف: | 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. |
| تدمد: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.00181.2009 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dca55049e9dcc28b635142b8b04df6e3 https://doi.org/10.1152/ajpregu.00181.2009 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....dca55049e9dcc28b635142b8b04df6e3 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15221490 03636119 |
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| DOI: | 10.1152/ajpregu.00181.2009 |