ReviewCurrent hypertension reports2016
The Role of CNS in the Effects of Salt on Blood Pressure.
Review in Current hypertension reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 12 citations in OpenAlex.
- Mineralocorticoid Receptor and Sleep Quality in Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Unraveling the gut microbiota's role in salt-sensitive hypertension: current evidences and future directions.Frontiers in cardiovascular medicine · 2024Review
- Central GαiFrontiers in endocrinology · 2022Review
- Article
- Sensory Afferent Renal Nerve Activated GαiFrontiers in physiology · 2021Article
- Effects of an SGLT2 inhibitor on the salt sensitivity of blood pressure and sympathetic nerve activity in a nondiabetic rat model of chronic kidney disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Review
- Role of Vasopressin in Rat Models of Salt-Dependent Hypertension.Current hypertension reports · 2017Review
- The Gut, Its Microbiome, and Hypertension.Current hypertension reports · 2017Review
- Genomic and rapid effects of aldosterone: what we know and do not know thus far.Heart failure reviews · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sympathetic nerve activity is involved in the pathogenesis of salt-sensitive hypertension. The central nervous system, which regulates sympathetic nerve activity and blood pressure, plays a pivotal role. Central sympathoexcitation is deeply involved in the pathogenesis of salt-sensitive hypertension, although the precise mechanisms have not been fully elucidated because of their complexity. The role of brain oxidative stress in sympathoexcitation has been suggested in some types of hypertensive animal models. We have shown that increased brain oxidative stress may elevate arterial pressure through central sympathoexcitation in salt-sensitive hypertension. Several other factors such as mineralocorticoid receptors, aldosterone, corticosterone, epithelial sodium channels, and angiotensin II also play important roles in central sympathetic activation, some of which can be associated with brain oxidative stress. Furthermore, brain paraventricular nucleus Gαi2-protein-mediated transduction has been recently reported as a candidate for the molecular mechanism countering the development of salt-sensitive hypertension.
Indexed as
Identifiers
What OpenQuestion holds
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.