ReviewCurrent hypertension reports2013
Neurogenic and sympathoexcitatory actions of NaCl in hypertension.
Review in Current hypertension reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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.
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.
Who cites it
44 citing papers in PubMed.
- High-salt intake alters autonomic maturation trajectories assessed by an HRV-based ANS Age Index in rats.Frontiers in physiology · 2026Article
- Sex differences in central salt sensing in the human brain.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Central nervous system mechanisms of salt-sensitive hypertension.Physiological reviews · 2025Review
- Silent Effects of High Salt: Risks Beyond Hypertension and Body's Adaptation to High Salt.Biomedicines · 2025Review
- Higher sodium in older individuals or after stroke/reperfusion, but not in migraine or Alzheimer's disease - a study in different preclinical models.Scientific reports · 2024Article
- Acute hypernatremia increases functional connectivity of NaCl sensing regions in the human brain: An fMRI pilot study.Autonomic neuroscience : basic & clinical · 2024Article
- Physiological Mechanisms of Dietary Salt Sensing in the Brain, Kidney, and Gastrointestinal Tract.Hypertension (Dallas, Tex. : 1979) · 2024Review
- A neural perspective on the treatment of hypertension: the neurological network excitation and inhibition (E/I) imbalance in hypertension.Frontiers in cardiovascular medicine · 2024Review
- Altered Neuronal Discharge in the Organum Vasculosum of the Lamina Terminalis Contributes to Dahl Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Dietary sodium and health: How much is too much for those with orthostatic disorders?Autonomic neuroscience : basic & clinical · 2022Review
- Central regulation of body fluid homeostasis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2022Review
- Central GαiFrontiers in endocrinology · 2022Review
- Sodium activates human monocytes via the NADPH oxidase and isolevuglandin formation.Cardiovascular research · 2021Article
- Salt sensitivity and hypertension.Journal of human hypertension · 2021Review
- Excessive salt consumption causes systemic calcium mishandling and worsens microarchitecture and strength of long bones in rats.Scientific reports · 2021Article
- Hypothalamic GPCR Signaling Pathways in Cardiometabolic Control.Frontiers in physiology · 2021Review
- Fetal Undernutrition Programming, Sympathetic Nerve Activity, and Arterial Hypertension Development.Frontiers in physiology · 2021Review
- Sensory Afferent Renal Nerve Activated GαiFrontiers in physiology · 2021Article
- Natriuresis During an Acute Intravenous Sodium Chloride Infusion in Conscious Sprague Dawley Rats Is Mediated by a Blood Pressure-Independent αFrontiers in physiology · 2021Article
- Sympathetic Nervous System Contributions to Hypertension: Updates and Therapeutic Relevance.The Canadian journal of cardiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Excess dietary salt intake is a major contributing factor to the pathogenesis of salt-sensitive hypertension. Strong evidence suggests that salt-sensitive hypertension is attributed to renal dysfunction, vascular abnormalities, and activation of the sympathetic nervous system. Indeed, sympathetic nerve transections or interruption of neurotransmission in various brain centers lowers arterial blood pressure (ABP) in many salt-sensitive models. The purpose of this article is to discuss recent evidence that supports a role of plasma or cerebrospinal fluid hypernatremia as a key mediator of sympathoexcitation and elevated ABP. Both experimental and clinical studies using time-controlled sampling have documented that a diet high in salt increases plasma and cerebrospinal fluid sodium concentration. To the extent it has been tested, acute and chronic elevations in sodium concentration activates the sympathetic nervous system in animals and humans. A further understanding of how the central nervous system detects changes in plasma or cerebrospinal fluid sodium concentration may lead to new therapeutic treatment strategies in salt-sensitive hypertension.
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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.