Evidence map›Paper›PMID 26883268›Full record

ArticleHypertension (Dallas, Tex. : 1979)2016

Inhibition of Nitric Oxide Synthase 1 Induces Salt-Sensitive Hypertension in Nitric Oxide Synthase 1α Knockout and Wild-Type Mice.

Ximing Wang, Kiran Chandrashekar, Lei Wang, En Yin Lai, Jin Wei, Gensheng Zhang, Shaohui Wang, Jie Zhang, Luis A Juncos, Ruisheng Liu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.3field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Salt sensitivity and hypertension.Journal of human hypertension · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. NaHCOHypertension (Dallas, Tex. : 1979) · 2019
    Article
  13. Article
  14. Knockout of NaAmerican journal of physiology. Renal physiology · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. Glucose dilates renal afferent arterioles via glucose transporter-1.American journal of physiology. Renal physiology · 2018
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Ximing WangFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
Kiran ChandrashekarFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
Lei WangFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
En Yin LaiFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
Jin WeiFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
Gensheng ZhangFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
Shaohui WangFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
Jie ZhangFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
Luis A JuncosFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.).
Ruisheng LiuFrom the Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa (X.W., L.W., J.W., G.Z., S.W., J.Z., R.L.); Shandong Medical Imaging Research Institute, Shandong Provincial Key Laboratory of Diagnosis and Treatment of Cardio-Cerebral Vascular Disease, Shandong University, Jinan, Shandong, China (X.W.); Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson (K.C., L.A.J.); and Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China (E.Y.L., G.Z.). ruisheng@health.usf.edu.
Florida College · USUniversity of Mississippi Medical Center · USUniversity of South Florida · USShandong University · CN

Funding

Tubuloglomerular feedback and salt-sensitive hypertensionR01DK098582 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2013 to 2016
$1.3M
Primary cilia and modulation of the renal microcirculationR01DK099276 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2014 to 2017
$980k
NIDDK NIH HHS DK098582NIDDK NIH HHS DK099276NIDDK NIH HHS R01 DK098582NIDDK NIH HHS R01 DK099276
6 · The paper itself

Abstract

We recently showed that α, β, and γ splice variants of neuronal nitric oxide synthase (NOS1) expressed in the macula densa and NOS1β accounts for most of the NO generation. We have also demonstrated that the mice with deletion of NOS1 specifically from the macula densa developed salt-sensitive hypertension. However, the global NOS1 knockout (NOS1KO) strain is neither hypertensive nor salt sensitive. This global NOS1KO strain is actually an NOS1αKO model. Consequently, we hypothesized that inhibition of NOS1β in NOS1αKO mice induces salt-sensitive hypertension. NOS1αKO and C57BL/6 wild-type (WT) mice were implanted with telemetry transmitters and divided into 7-nitroindazole (10 mg/kg/d)-treated and nontreated groups. All of the mice were fed a normal salt (0.4% NaCl) diet for 5 days, followed by a high-salt diet (4% NaCl). NO generation by the macula densa was inhibited by >90% in WT and NOS1αKO mice treated with 7-nitroindazole. Glomerular filtration rate in conscious mice was increased by ≈ 40% after a high-salt diet in both NOS1αKO and WT mice. In response to acute volume expansion, glomerular filtration rate, diuretic and natriuretic response were significantly blunted in the WT and knockout mice treated with 7-nitroindazole. Mean arterial pressure had no significant changes in mice fed a high-salt diet, but increased ≈ 15 mm Hg similarly in NOS1αKO and WT mice treated with 7-nitroindazole. We conclude that NOS1β, but not NOS1α, plays an important role in control of sodium excretion and hemodynamics in response to either an acute or a chronic salt loading.

Indexed as

Analysis of VarianceAnimalsArterial PressureBlotting, WesternCells, CulturedDisease Models, AnimalGlomerular Filtration RateHypertensionMiceMice, Inbred C57BLMice, KnockoutNitric Oxide Synthase Type IRandom AllocationReal-Time Polymerase Chain ReactionSensitivity and SpecificitySodium Chloride, DietaryNitric Oxide Synthase Type ISodium Chloride, Dietary7-nitroindazolearterial pressurehypertensionsodiumtelemetry

Identifiers

PMID26883268
PMCPMC4802158
OpenAlexW2286283267

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.