Evidence map›Paper›PMID 21937997›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2011

Angiotensin-converting enzyme inhibition, but not AT(1) receptor blockade, in the solitary tract nucleus improves baroreflex sensitivity in anesthetized transgenic hypertensive (mRen2)27 rats.

Katsunori Isa, Amy C Arnold, Brian M Westwood, Mark C Chappell, Debra I Diz

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2011. 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
2.7field-weighted citation impact, top 9% 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, 25 citations in OpenAlex.

  1. New insights and predictability from in vivo recordings of paroxysmal sympathetic hyperactivity in disorders of consciousness.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Novel role of aminopeptidase-A in angiotensin-(1-7) metabolism post myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2014
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Brain renin-angiotensin system in the nexus of hypertension and aging.Hypertension research : official journal of the Japanese Society of Hypertension · 2013
    Review
  12. Review
  13. Article
  14. Article
  15. Angiotensin peptides and central autonomic regulation.Current opinion in pharmacology · 2011
    Review
  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 1 institution in 1 country.

Katsunori IsaHypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1032, USA.
Amy C Arnold
Brian M Westwood
Mark C Chappell
Debra I Diz
Wake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 1994 to 2019
$34.8M
Estrogen, ACE2 and Salt-SensitivityR01HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 2004 to 2008
$1.6M
REGULATION AND FUNCTION OF ANGIOTENSIN (1-7)R29HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 1996 to 1999
–
NHLBI NIH HHS HL51952NHLBI NIH HHS HL56973NHLBI NIH HHS P01 HL051952NHLBI NIH HHS R29 HL056973
6 · The paper itself

Abstract

Transgenic hypertensive (mRen2)27 rats overexpress the murine Ren2 gene and have impaired baroreflex sensitivity (BRS) for control of the heart rate. Removal of endogenous angiotensin (Ang)-(1-7) tone using a receptor blocker does not further lower BRS. Therefore, we assessed whether blockade of Ang II with a receptor antagonist or combined reduction in Ang II and restoration of endogenous Ang-(1-7) levels with Ang-converting enzyme (ACE) inhibition will improve BRS in these animals. Bilateral solitary tract nucleus (nTS) microinjections of the AT(1) receptor blocker, candesartan (CAN, 24 pmol in 120 nl, n=9), or a peptidic ACE inhibitor, bradykinin (BK) potentiating nonapeptide (Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro; BPP9α, 9 nmol in 60 nl, n=12), in anesthetized male (mRen2)27 rats (15-25 weeks of age) show that AT(1) receptor blockade had no significant effect on BRS, whereas microinjection of BPP9α improved BRS over 60-120 min. To determine whether Ang-(1-7) or BK contribute to the increase in BRS, separate experiments using the Ang-(1-7) receptor antagonist D-Ala(7)-Ang-(1-7) or the BK antagonist HOE-140 showed that only the Ang-(1-7) receptor blocker completely reversed the BRS improvement. Thus, acute AT(1) blockade is unable to reverse the effects of long-term Ang II overexpression on BRS, whereas ACE inhibition restores BRS over this same time frame. As the BPP9α potentiation of BK actions is a rapid phenomenon, the likely mechanism for the observed delayed increase in BRS is through ACE inhibition and elevation of endogenous Ang-(1-7).

Indexed as

AnesthesiaAngiotensin-Converting Enzyme InhibitorsAngiotensin IAngiotensin II Type 1 Receptor BlockersAnimalsBaroreflexBenzimidazolesBiphenyl CompoundsBlood PressureBradykininBradykinin Receptor AntagonistsHeart RateHypertensionMaleMicroinjectionsOligopeptidesAngiotensin-Converting Enzyme InhibitorsAngiotensin Iangiotensin I (1-7)Angiotensin II Type 1 Receptor BlockersArg-Pro-Gln-Ile-Pro-ProBenzimidazolesBiphenyl CompoundsBradykininBradykinin Receptor AntagonistscandesartanOligopeptidesPeptide FragmentsTetrazoles

Identifiers

PMID21937997
PMCPMC4160904
OpenAlexW2084602333

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.