Evidence map›Paper›PMID 19717492›Full record

ReviewExperimental physiology2010

Region-specific changes in sympathetic nerve activity in angiotensin II-salt hypertension in the rat.

John W Osborn, Gregory D Fink

Open access · greenAbstract readReview
In one paragraph

Review in Experimental physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 102 citations in OpenAlex.

  1. Special Issue: Recent Research on Hypertension and Related Complications.International journal of molecular sciences · 2026
    Article
  2. Article
  3. Review
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  5. Article
  6. Multi-Organ Denervation: The Past, Present and Future.Journal of clinical medicine · 2025
    Review
  7. Article
  8. Article
  9. Article
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  11. Article
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  14. Article
  15. Review
  16. Review
  17. Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  18. Article
  19. The Role of Renin-Angiotensin-Aldosterone System and Its New Components in Arterial Stiffness and Vascular Aging.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2018
    Review
  20. Review
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

2 authors at 2 institutions in 1 country.

John W OsbornDepartment of Integrative Biology and Physiology, University of Minnesota, Room 6-125 Jackson Hall, Minneapolis, MN 55455, USA. osbor003@umn.edu
Gregory D Fink
Michigan State University · USUniversity of Minnesota · US

Funding

Long-Term Neural Determinants of Cardiovascular DiseasesR01HL076312 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI OSBORN, JOHN W · 2005 to 2009
$5.6M
NHLBI NIH HHS R01 HL076312NHLBI NIH HHS R01HL076312
6 · The paper itself

Abstract

It is now well accepted that many forms of experimental hypertension and human essential hypertension are caused by increased activity of the sympathetic nervous system. However, the role of region-specific changes in sympathetic nerve activity (SNA) in the pathogenesis of hypertension has been difficult to determine because methods for chronic measurement of SNA in conscious animals have not been available. We have recently combined indirect, and continuous and chronic direct, assessment of region-specific SNA to characterize hypertension produced by administration of angiotensin II (Ang II) to rats consuming a high-salt diet (Ang II-salt hypertension). Angiotensin II increases whole-body noradrenaline (NA) spillover and depressor responses to ganglionic blockade in rats consuming a high-salt diet, but not in rats on a normal-salt diet. Despite this evidence for increased 'whole-body SNA' in Ang II-salt hypertensive rats, renal SNA is decreased in this model and renal denervation does not attenuate the steady-state level of arterial pressure. In addition, neither lumbar SNA, which largely targets skeletal muscle, nor hindlimb NA spillover is changed from control levels in Ang II-salt hypertensive rats. However, surgical denervation of the splanchnic vascular bed attenuates/abolishes the increase in arterial pressure and total peripheral resistance, as well as the decrease in vascular capacitance, observed in Ang II-salt hypertensive rats. We hypothesize that the 'sympathetic signature' of Ang II-salt hypertension is characterized by increased splanchnic SNA, no change in skeletal muscle SNA and decreased renal SNA, and this sympathetic signature creates unique haemodynamic changes capable of producing sustained hypertension.

Indexed as

Disease Models, AnimalAngiotensin IIAnimalsHumansHypertensionKidneyMuscle, SkeletalRatsSodium Chloride, DietarySympathetic Nervous SystemVisceraAngiotensin IISodium Chloride, Dietary

Identifiers

PMID19717492
PMCPMC2856071
OpenAlexW1935889229

What OpenQuestion holds

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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.