Evidence map›Paper›PMID 22581746›Full record

ArticleExperimental physiology2012

A role for nitric oxide within the nucleus tractus solitarii in the development of muscle mechanoreflex dysfunction in hypertension.

Anna K Leal, Megan N Murphy, Gary A Iwamoto, Jere H Mitchell, Scott A Smith

Open access · bronzeAbstract read
In one paragraph

Article in Experimental physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The exercise pressor reflex: An update.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2022
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
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

5 authors at 3 institutions in 2 countries.

Anna K LealDepartment of Bioengineering, University of Texas Southwestern Medical Center, Dallas, TX 75390-9174, USA.
Megan N Murphy
Gary A Iwamoto
Jere H Mitchell
Scott A Smith
The University of Texas Southwestern Medical Center · USAmerican Physical Therapy Association · USBioengineering Center · RU

Funding

Mechanisms of Exercise Pressor Reflex Overactivity in HypertensionR01HL088422 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SMITH, SCOTT A · 2008 to 2012
$2.0M
Role of Thromboxane in the Exercise Pressor Reflex in Peripheral Artery DiseaseF32HL108406 · NHLBI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI LEAL, ANNA KATHERINE · 2011 to 2013
$143k
Pathogenesis of Exercise Pressor Reflex Dysfunction in HypertensionF31HL094075 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI LEAL, ANNA KATHERINE · 2008 to 2008
$26k
NHLBI NIH HHS F31 HL094075NHLBI NIH HHS F32 HL108406NHLBI NIH HHS HL-088422NHLBI NIH HHS HL-094075NHLBI NIH HHS R01 HL088422
6 · The paper itself

Abstract

Evidence suggests that the muscle mechanoreflex, a circulatory reflex that raises blood pressure and heart rate (HR) upon activation of mechanically sensitive afferent fibres in skeletal muscle, is overactive in hypertension. However, the mechanisms underlying this abnormal reflex function have yet to be identified. Sensory input from the mechanoreflex is processed within the nucleus tractus solitarii (NTS) in the medulla oblongata. Within the NTS, the enzymatic activity of nitric oxide synthase produces nitric oxide (NO). This centrally derived NO has been shown to modulate muscle reflex activity and serves as a viable candidate for mediating the mechanoreflex dysfunction that develops in hypertension. We hypothesized that mechanoreflex dysfunction in hypertension is mediated by abnormal alterations in NO production in the NTS. Mechanically sensitive afferent fibres were stimulated by passively stretching hindlimb muscle before and after blocking the endogenous production of NO within the NTS via microdialysis of the NO synthase inhibitor L-NAME (1 and 5 mM) in normotensive Wistar-Kyoto rats and spontaneously hypertensive rats (SHRs). Changes in HR and mean arterial pressure in response to stretch were significantly larger in SHRs compared with Wistar-Kyoto rats prior to L-NAME dialysis. Attenuating NO production via L-NAME in normotensive rats recapitulated the exaggerated cardiovascular response to stretch observed in SHRs. Dialysing L-NAME in SHRs further accentuated the increases in HR and mean arterial pressure elicited by stretch. These findings support the contention that reductions in NO production within the NTS contribute to the generation of abnormal cardiovascular control by the skeletal muscle mechanoreflex in hypertension.

Indexed as

Blood PressureMechanotransduction, CellularReflex, StretchAnimalsDisease Models, AnimalEnzyme InhibitorsGanglionic BlockersHeart RateHexamethoniumHypertensionMaleMicrodialysisMuscle, SkeletalMuscle SpindlesNG-Nitroarginine Methyl EsterNitric OxideEnzyme InhibitorsGanglionic BlockersHexamethoniumNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase

Identifiers

PMID22581746
PMCPMC3480555
OpenAlexW2112467987

What OpenQuestion holds

Textmetadata
LicenceTDM
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.