Evidence map›Paper›PMID 10790160›Full record

ArticleThe Journal of physiology2000

Endothelin-1 and photoreleased diacylglycerol increase L-type Ca2+ current by activation of protein kinase C in rat ventricular myocytes.

J Q He, Y Pi, J W Walker, T J Kamp

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 80 citations in OpenAlex.

  1. αeLife · 2023
    Article
  2. IPAmerican journal of physiology. Heart and circulatory physiology · 2021
    Article
  3. A new stone for a new path, from "physiology to the bedside".Pflugers Archiv : European journal of physiology · 2019
    Article
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  6. Review
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  8. Review
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  11. Article
  12. Review
  13. Article
  14. Article
  15. Regulation of cardiac excitability by protein kinase C isozymes.Frontiers in bioscience (Scholar edition) · 2012
    Review
  16. Article
  17. The cardiovascular physiology and pharmacology of endothelin-1.Advances in pharmacology (San Diego, Calif.) · 2010
    Review
  18. Article
  19. Review
  20. Endothelin-1 regulates cardiac L-type calcium channels via NAD(P)H oxidase-derived superoxide.The Journal of pharmacology and experimental therapeutics · 2008
    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.

J Q HeDepartment of Medicine, University of Wisconsin-Madison, Madison, WI 53792, USA.
Y Pi
J W Walker
T J Kamp
University of Wisconsin–Madison · US

Funding

RYANODINE RECEPTORS AND ACCESSORY PROTEINSP01HL047053 · NHLBI · UNIVERSITY OF WISCONSIN MADISON · PI MOSS, RICHARD L · 1995 to 2004
$8.5M
NHLBI NIH HHS P01 HL047053NHLBI NIH HHS P01HL47053
6 · The paper itself

Abstract

The amphotericin B-perforated whole-cell patch clamp technique was used to determine the modulation of L-type Ca2+ channels by protein kinase C (PKC)-mediated pathways in adult rat ventricular myocytes. Application of 10 nM endothelin-1 (ET-1) increased peak Ca2+ current (ICa) by 28.2 +/- 2.5 % (n = 13) and slowed current decay. These effects were prevented by the endothelin receptor antagonist PD145065 (10 microM) and by the PKC inhibitor chelerythrine (8 microM). To establish if direct activation of PKC mimicked the ET-1 effect, the active and inactive phorbol esters (phorbol-12-myristate-13-acetate and 4alpha-phorbol-12, 13-didecanoate) were tested. Both phorbol esters (100 nM) resulted in a small (approximately 10%) increase in ICa, suggesting PKC-independent effects. Bath application of dioctanoylglycerol (diC8), a diacylglycerol (DAG) analogue which is capable of directly activating PKC, caused a gradual decline in peak ICa (50.4 +/- 6.2 %, n = 5) and increased the rate of current decay. These effects were unaffected by the PKC inhibitor chelerythrine (8 microM). Intracellular photorelease of caged diC8 with 3 or 10 s exposure to UV light produced a concentration-dependent increase in peak ICa (20. 7 +/- 8.5 % (n = 8) for 3 s UV and 60.8 +/- 11.4 % (n = 13) for 10 s UV), which could be inhibited by chelerythrine. Our results demonstrate that both ET-1 and intracellularly photoreleased diC8 increase ICa by a PKC-mediated pathway, which is in direct contrast to the PKC-independent inhibition of ICa produced by bath-applied diC8. We conclude that specific cellular pools of DAG are crucially important in the regulation of ICa by PKC.

Indexed as

AlkaloidsAnimalsBenzophenanthridinesCadmiumCalciumCalcium Channel BlockersCalcium Channels, L-TypeCarcinogensDiglyceridesElectrophysiologyEndothelin-1Enzyme InhibitorsMaleMembrane PotentialsMuscle Fibers, SkeletalMyocardium1,2-dioctanoylglycerolAlkaloidsBenzophenanthridinesCadmiumCalciumCalcium Channel BlockersCalcium Channels, L-TypeCarcinogenschelerythrineDiglyceridesEndothelin-1Enzyme InhibitorsNifedipinePhenanthridinesProtein Kinase CTetradecanoylphorbol Acetate

Identifiers

PMID10790160
PMCPMC2269902
OpenAlexW2085992470

What OpenQuestion holds

Textmetadata
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.