Evidence map›Paper›PMID 27001546›Full record

ArticleInternational journal of obesity (2005)2016

Sympathetic hyper-excitation in obesity and pulmonary hypertension: physiological relevance to the 'obesity paradox'.

C Diong, P P Jones, H Tsuchimochi, E A Gray, G Hughes, T Inagaki, C T Bussey, Y Fujii, K Umetani, M Shirai and 1 more

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Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

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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

11 authors at 3 institutions in 2 countries.

C DiongDepartment of Physiology-HeartOtago, University of Otago, Dunedin, New Zealand.
P P JonesDepartment of Physiology-HeartOtago, University of Otago, Dunedin, New Zealand.
H TsuchimochiDepartment of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
E A GrayDepartment of Physiology-HeartOtago, University of Otago, Dunedin, New Zealand.
G HughesDepartment of Physiology-HeartOtago, University of Otago, Dunedin, New Zealand.
T InagakiDepartment of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
C T BusseyDepartment of Physiology-HeartOtago, University of Otago, Dunedin, New Zealand.
Y FujiiDepartment of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
K UmetaniJapan Synchrotron Radiation Research Institute, Hyogo, Japan.
M ShiraiDepartment of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
D O SchwenkeDepartment of Physiology-HeartOtago, University of Otago, Dunedin, New Zealand.
University of Otago · NZNational Cerebral and Cardiovascular Center · JPJapan Synchrotron Radiation Research Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWithin the lung, sympathetic nerve activity (SNA) has an important role in facilitating pulmonary vasodilation. As SNA is elevated in obesity, we aimed to assess the impact of sympathetic hyper-excitation on pulmonary vascular homeostasis in obesity, and its potential role in ameliorating the severity of pulmonary hypertension (PH); the well-documented 'obesity paradox' phenomenon.

methodsZucker obese and lean rats were exposed to normoxia or chronic hypoxia (CH-10% O2) for 2 weeks. Subsequently, pulmonary SNA (pSNA) was recorded (electrophysiology), or the pulmonary microcirculation was visualized using Synchrotron microangiography. Acute hypoxic pulmonary vasoconstriction (HPV) was assessed before and after blockade of β1-adrenergic receptors (ARs) (atenolol, 3 mg kg(-1)) and β1+β2-adrenergic (propranolol, 2 mg kg(-1)).

resultspSNA of normoxic obese rats was higher than lean counterparts (2.4 and 0.5 μV s, respectively). SNA was enhanced following the development of PH in lean rats, but more so in obese rats (1.7 and 6.8 μV s, respectively). The magnitude of HPV was similar for all groups (for example, ~20% constriction of the 200-300 μm vessels). Although β-blockade did not modify HPV in lean rats, it significantly augmented the HPV in normoxic obese rats (β1 and β2 blockade), and more so in obese rats with PH (β2-blockade alone). Western blots showed, while the expression of pulmonary β1-ARs was similar for all rats, the expression of β2-ARs was downregulated in obesity and PH.

conclusionsThis study suggests that sympathetic hyper-excitation in obesity may have an important role in constraining the severity of PH and, thus, contribute in part to the 'obesity paradox' in PH.

Indexed as

Adrenergic beta-AntagonistsAnimalsDisease Models, AnimalHypertension, PulmonaryHypoxiaLungMicrocirculationObesityPropranololRatsRats, ZuckerSympathetic Nervous SystemVasoconstrictionAdrenergic beta-AntagonistsPropranolol

Identifiers

PMID27001546
OpenAlexW2279479921

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.