ArticleClinical and experimental pharmacology & physiology2013
Distinct regulation of inner medullary collecting duct nitric oxide production from mice and rats.
Article in Clinical and experimental pharmacology & physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021Article
- Collecting Duct Nitric Oxide Synthase 1ß Activation Maintains Sodium Homeostasis During High Sodium Intake Through Suppression of Aldosterone and Renal Angiotensin II Pathways.Journal of the American Heart Association · 2017Article
- Collecting duct-specific knockout of nitric oxide synthase 3 impairs water excretion in a sex-dependent manner.American journal of physiology. Renal physiology · 2016Article
- High salt intake increases endothelin B receptor function in the renal medulla of rats.Life sciences · 2016Article
- High salt induces autocrine actions of ET-1 on inner medullary collecting duct NO production via upregulated ETB receptor expression.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Dynamin-2 is a novel NOS1β interacting protein and negative regulator in the collecting duct.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- NOS1-dependent negative feedback regulation of the epithelial sodium channel in the collecting duct.American journal of physiology. Renal physiology · 2015Article
- Molecular mechanisms of neuronal nitric oxide synthase in cardiac function and pathophysiology.The Journal of physiology · 2014Review
- Female sex hormones protect against salt-sensitive hypertension but not essential hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Renal collecting duct NOS1 maintains fluid-electrolyte homeostasis and blood pressure.Hypertension (Dallas, Tex. : 1979) · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Nitric oxide (NO) and NO synthase 1 (NOS1) maintain sodium and water homeostasis. The NOS1α and NOS1β splice variants are expressed in the rat inner medulla, but only NOS1β is expressed in the mouse. Collecting duct NOS1 is necessary for blood pressure control. We hypothesized that NOS1 splice variant expression and NO production in the inner medullary collecting duct (IMCD) are regulated differently in mice and rats by high dietary sodium. Male C57blk/J6 mice and Sprague-Dawley rats were fed a 0.4% (normal salt; NS), or 4% (high salt; HS) NaCl diet for 2 or 7 days. Mean arterial pressure was not altered by HS, whereas urinary sodium excretion in mice and rats was increased significantly. Urinary excretion of nitrate/nitrite (NO(x)) and IMCD nitrite production were significantly greater in mice compared with rats on the HS diet. Western blotting indicated that only NOS1β and NOS3 were expressed in the mouse IMCD and that expression was unaffected by the HS diet at either time point. In contrast, NOS1α was detected in the IMCD of rats, in addition to NOS1β and NOS3. Feeding of the HS diet for 2 days increased NOS1α and NOS1β expression in the rat IMCD and 7 day feeding of the HS diet further increased NOS1β expression. Expression of NOS3 was unchanged by the HS diet at either time point. In conclusion, IMCD NO production in mice and rats is distinctly regulated under both NS and HS conditions, including expression of NOS1 splice variants.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.