Evidence map›Paper›PMID 30095973›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2018

Regulation of sympathetic vasomotor activity by the hypothalamic paraventricular nucleus in normotensive and hypertensive states.

Roger A Dampney, Lisete C Michelini, De-Pei Li, Hui-Lin Pan

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

99 citing papers in PubMed, 143 citations in OpenAlex.

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  10. Single-nucleus RNA sequencing reveals Cntnap2Journal of advanced research · 2026
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39 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 3 countries.

Roger A DampneyDepartment of Physiology, University of Sydney , Sydney, New South Wales , Australia.
Lisete C MicheliniDepartment of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo , São Paulo , Brazil.
De-Pei LiDepartment of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center , Houston, Texas.
Hui-Lin PanDepartment of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center , Houston, Texas.
The University of Texas MD Anderson Cancer Center · USUniversidade de São Paulo · BRUniversity of Sydney · AU

Funding

Signaling Mechanisms of CNS Neuronal Plasticity in HypertensionR01HL131161 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PAN, HUI-LIN · 2016 to 2019
$2.1M
Mechanisms of Stress-Induced HypertensionR01HL139523 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, DE-PEI, PAN, HUI-LIN · 2018 to 2021
$1.8M
NHLBI NIH HHS R01 HL131161NHLBI NIH HHS R01 HL139523
6 · The paper itself

Abstract

The hypothalamic paraventricular nucleus (PVN) is a unique and important brain region involved in the control of cardiovascular, neuroendocrine, and other physiological functions pertinent to homeostasis. The PVN is a major source of excitatory drive to the spinal sympathetic outflow via both direct and indirect projections. In this review, we discuss the role of the PVN in the regulation of sympathetic output in normal physiological conditions and in hypertension. In normal healthy animals, the PVN presympathetic neurons do not appear to have a major role in sustaining resting sympathetic vasomotor activity or in regulating sympathetic responses to short-term homeostatic challenges such as acute hypotension or hypoxia. Their role is, however, much more significant during longer-term challenges, such as sustained water deprivation, chronic intermittent hypoxia, and pregnancy. The PVN also appears to have a major role in generating the increased sympathetic vasomotor activity that is characteristic of multiple forms of hypertension. Recent studies in the spontaneously hypertensive rat model have shown that impaired inhibitory and enhanced excitatory synaptic inputs to PVN presympathetic neurons are the basis for the heightened sympathetic outflow in hypertension. We discuss the molecular mechanisms underlying the presynaptic and postsynaptic alterations in GABAergic and glutamatergic inputs to PVN presympathetic neurons in hypertension. In addition, we discuss the ability of exercise training to correct sympathetic hyperactivity by restoring blood-brain barrier integrity, reducing angiotensin II availability, and decreasing oxidative stress and inflammation in the PVN.

Indexed as

Blood PressureSynaptic TransmissionAngiotensin IIAnimalsBlood-Brain BarrierCardiovascular SystemDisease Models, AnimalExcitatory Postsynaptic PotentialsExercise TherapyGABAergic NeuronsGlutamic AcidHumansHypertensionInflammation MediatorsNeural InhibitionOxidative StressAngiotensin IIGlutamic AcidInflammation Mediatorsautonomic nervous systemhypothalamusparaventricular nucleussympathetic nervous systemsynaptic plasticitysynaptic transmission

Identifiers

PMID30095973
PMCPMC6297824
OpenAlexW2886129647

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.