ArticleHypertension (Dallas, Tex. : 1979)2017
Blood Pressure in Healthy Humans Is Regulated by Neuronal NO Synthase.
Article in Hypertension (Dallas, Tex. : 1979), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Characterization of theMolecules (Basel, Switzerland) · 2024Trial
- The Effect of a Neuronal Nitric Oxide Synthase Inhibitor on Neurovascular Regulation in Humans.Circulation research · 2022Trial
- Neuronal nitric oxide synthase regulates regional brain perfusion in healthy humans.Cardiovascular research · 2022Trial
- Does l-citrulline supplementation improve exercise blood flow in older adults?Experimental physiology · 2017Trial
- Substance P regulates Tacr1 neurons, which control nitric oxide-mediated neurovascular coupling in the mouse cortex.Science advances · 2026Article
- Brain nitric oxide and inflammation in chronic intermittent hypoxia: Contributors to cognitive impairment and hypertension.Brain, behavior, & immunity - health · 2025Review
- Morphometric and Molecular Interplay in Hypertension-Induced Cardiac Remodeling with an Emphasis on the Potential Therapeutic Implications.International journal of molecular sciences · 2025Review
- Molecular modelling of fullerene CScientific reports · 2024Article
- Adrenoceptors and Hypertension.Handbook of experimental pharmacology · 2024Review
- Dysfunctional and Dysregulated Nitric Oxide Synthases in Cardiovascular Disease: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2023Review
- A cardiac-null mutation of Prdm16 causes hypotension in mice with cardiac hypertrophy via increased nitric oxide synthase 1.PloS one · 2022Article
- Oxidative Stress, GTPCH1, and Endothelial Nitric Oxide Synthase Uncoupling in Hypertension.Antioxidants & redox signaling · 2021Review
- Nitric Oxide Synthase Inhibitors into the Clinic at Last.Handbook of experimental pharmacology · 2021Article
- Role of neuronal nitric oxide synthase on cardiovascular functions in physiological and pathophysiological states.Nitric oxide : biology and chemistry · 2020Review
- Impact of adipokines and myokines on fat browning.Journal of physiology and biochemistry · 2020Review
- (-)-Epicatechin Reduces the Blood Pressure of Young Borderline Hypertensive Rats During the Post-Treatment Period.Antioxidants (Basel, Switzerland) · 2020Article
- Review
- Pattern of sympathetic vasomotor activity in a model of hypertension induced by nitric oxide synthase blockade.Physiological reports · 2019Article
- Angiotensin II, dopamine and nitric oxide. An asymmetrical neurovisceral interaction between brain and plasma to regulate blood pressure.AIMS neuroscience · 2019Article
- Flow does not alter eNOS phosphoryation at Ser1179 or Thr495 in preconstricted mouse mesenteric arteries.Physiological reports · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
NO is physiologically generated by endothelial and neuronal NO synthase (nNOS) isoforms. Although nNOS was first identified in brain, it is expressed in other tissues, including perivascular nerves, cardiac and skeletal muscle. Increasing experimental evidence suggests that nNOS has important effects on cardiovascular function, but its composite effects on systemic hemodynamics in humans are unknown. We undertook the first human study to assess the physiological effects of systemic nNOS inhibition on basal hemodynamics. Seventeen healthy normotensive men aged 24±4 years received acute intravenous infusions of an nNOS-selective inhibitor, S-methyl-l-thiocitrulline, and placebo on separate occasions. An initial dose-escalation study showed that S-methyl-l-thiocitrulline (0.1-3.0 µmol/kg) induced dose-dependent changes in systemic hemodynamics. The highest dose of S-methyl-l-thiocitrulline (3.0 µmol/kg over 10 minutes) significantly increased systemic vascular resistance (+42±6%) and diastolic blood pressure (67±1 to 77±3 mm Hg) when compared with placebo (both
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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 OpenQuestion graph.