ArticleAmerican journal of physiology. Renal physiology2015
NOS1-dependent negative feedback regulation of the epithelial sodium channel in the collecting duct.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Endothelial histone deacetylase 1 activity impairs kidney microvascular NO signaling in rats fed a high-salt diet.Acta physiologica (Oxford, England) · 2024Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Genetic Modifications to Alter Blood Pressure Level.Biomedicines · 2022Review
- Kidney-specific KO of the circadian clock protein PER1 alters renal NaAmerican journal of physiology. Renal physiology · 2022Article
- Role of collecting duct principal cell NOS1β in sodium and potassium homeostasis.Physiological reports · 2021Article
- nNOS regulates ciliated cell polarity, ciliary beat frequency, and directional flow in mouse trachea.Life science alliance · 2021Article
- High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021Article
- Failure to vasodilate in response to salt loading blunts renal blood flow and causes salt-sensitive hypertension.Cardiovascular research · 2021Article
- Interplay of the Circadian Clock and Endothelin System.Physiology (Bethesda, Md.) · 2021Review
- Knockout of the circadian clock protein PER1 results in sex-dependent alterations of ET-1 production in mice in response to a high-salt diet plus mineralocorticoid treatment.Canadian journal of physiology and pharmacology · 2020Article
- Sensing of tubular flow and renal electrolyte transport.Nature reviews. Nephrology · 2020Review
- The contribution of collecting duct NOS1 to the concentrating mechanisms in male and female mice.American journal of physiology. Renal physiology · 2019Article
- Nephron-Specific Disruption of Nitric Oxide Synthase 3 Causes Hypertension and Impaired Salt Excretion.Journal of the American Heart Association · 2018Article
- Epithelial NaAnnual review of physiology · 2018Review
- Nitric oxide production by glomerular podocytes.Nitric oxide : biology and chemistry · 2018Article
- High dietary sodium causes dyssynchrony of the renal molecular clock in rats.American journal of physiology. Renal physiology · 2018Article
- 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
- Renal denervation attenuates hypertension but not salt sensitivity in ETAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Role for reactive oxygen species in flow-stimulated inner medullary collecting duct endothelin-1 production.American journal of physiology. Renal physiology · 2017Article
- Desoxycorticosterone pivalate-salt treatment leads to non-dipping hypertension in Per1 knockout mice.Acta physiologica (Oxford, England) · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
With an increase in urine flow there is a significant increase in shear stress against the renal epithelium including the inner medullary collecting duct, resulting in an increase in nitric oxide (NO) production. The mechanisms of the shear stress-mediated increases in NO are undetermined. Previous studies found that shear stress increases epithelial sodium channel (ENaC) open probability and endothelin (ET)-1 production in an ENaC-dependent mechanism in the collecting duct (CD). Given that ET-1 stimulates NO production in the CD, we hypothesized that shear stress-induced NO production is downstream of shear stress-induced ENaC activation and ET-1 production in a negative feedback loop. We determined that nitric oxide synthase 1 (NOS1) and NOS3 contribute to shear stress-mediated NO production in the CD, that is attenuated by low doses of the ENaC inhibitors amiloride and benzamil. Moreover, ETB receptor blockade significantly blunted the shear stress-mediated NO production. We further elucidated whether mice lacking NOS1 in the collecting duct (CDNOS1KO) have an impaired renal ET-1 system in the CD. Although urinary ET-1 production and inner medullary ET receptor expression were similar between flox control and CDNOS1KO mice, acute ET-1 treatment significantly reduced ENaC open probability in CDs from flox mice but not CDNOS1KO mice compared with basal. Basal ENaC activity in CDs was similar between the genotypes. We conclude that during acute shear stress across the CD, ENaC acts in a negative feedback loop to stimulate NO production in an ETB/NOS1-dependent manner resulting in a decrease in ENaC open probability and promoting natriuresis.
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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 OpenQuestion graph.