Evidence map›Paper›PMID 26537343›Full record

ArticlePhysiological reports2015

BDNF contributes to angiotensin II-mediated reductions in peak voltage-gated K+ current in cultured CATH.a cells.

Bryan K Becker, Han-Jun Wang, Changhai Tian, Irving H Zucker

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Depression and Cardiovascular Disease: The Viewpoint of Platelets.International journal of molecular sciences · 2020
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Within the Brain: The Renin Angiotensin System.International journal of molecular sciences · 2018
    Review
  12. Article
  13. 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

4 authors at 1 institution in 1 country.

Bryan K BeckerCellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.
Han-Jun WangCellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.
Changhai TianCellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.
Irving H ZuckerCellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska izucker@unmc.edu.
University of Nebraska Medical Center · US

Funding

The Role of Excitatory Input into the PVN on Increased Sympathetic Drive in HeartP01HL062222 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PATEL, KAUSHIK P · 1999 to 2019
$32.2M
Molecular and Cellular Determinants of the Exercise Pressor Reflex in CHFR01HL116608 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI ZUCKER, IRVING H · 2013 to 2016
$1.8M
Brain-Derived Neurotrophic Factor and Sympathoexcitation in Chronic Heart FailureF31HL126286 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BECKER, BRYAN K · 2015 to 2015
$18k
NHLBI NIH HHS F31 HL126286NHLBI NIH HHS P01 HL062222NHLBI NIH HHS R01 HL116608
6 · The paper itself

Abstract

Increased central angiotensin II (Ang II) levels contribute to sympathoexcitation in cardiovascular disease states such as chronic heart failure and hypertension. One mechanism by which Ang II increases neuronal excitability is through a decrease in voltage-gated, rapidly inactivating K(+) current (IA); however, little is known about how Ang II signaling results in reduced IA. Brain-derived neurotrophic factor (BDNF) has also been demonstrated to decrease IA and has signaling components common to Ang II. Therefore, we hypothesized that Ang II-mediated suppression of voltage-gated K(+) currents is due, in part, to BDNF signaling. Differentiated CATH.a, catecholaminergic cell line treated with BDNF for 2 h exhibited a reduced IA in a manner similar to that of Ang II treatment as demonstrated by whole-cell patch-clamp analysis. Inhibiting BDNF signaling by pretreating neurons with an antibody against BDNF significantly attenuated the Ang II-induced reduction of IA. Inhibition of a common component of both BDNF and Ang II signaling, p38 MAPK, with SB-203580 attenuated the BDNF-mediated reductions in IA. These results implicate the involvement of BDNF signaling in Ang II-induced reductions of IA, which may cause increases in neuronal sensitivity and excitability. We therefore propose that BDNF may be a necessary component of the mechanism by which Ang II reduces IA in CATH.a cells.

Indexed as

AT1Rp38 MAPKSB‐203580TrkB

Identifiers

PMID26537343
PMCPMC4673628
OpenAlexW2180099536

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.