Evidence map›Paper›PMID 23118129›Full record

ArticleCardiovascular research2013

SKA-31, a novel activator of SK(Ca) and IK(Ca) channels, increases coronary flow in male and female rat hearts.

Ramesh C Mishra, Darrell Belke, Heike Wulff, Andrew P Braun

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. CaInternational journal of molecular sciences · 2023
    Review
  2. Review
  3. KPflugers Archiv : European journal of physiology · 2021
    Article
  4. SKA-31, an activator of CaPharmacological research · 2020
    Article
  5. Article
  6. Pharmacologic targeting of endothelial CaChannels (Austin, Tex.) · 2018
    Review
  7. Impact of Aging on Calcium Signaling and Membrane Potential in Endothelium of Resistance Arteries: A Role for Mitochondria.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017
    Article
  8. Protective role of ACE2-Ang-(1-7)-Mas in myocardial fibrosis by downregulating KPflugers Archiv : European journal of physiology · 2016
    Article
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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 2 institutions in 2 countries.

Ramesh C MishraDepartment of Physiology and Pharmacology, Faculty of Medicine, University of Calgary, 3330 Hospital Dr. NW, Calgary, AB, Canada T2N 4N1.
Darrell Belke
Heike Wulff
Andrew P Braun
University of Calgary · CAUniversity of California, Davis · US

Funding

Optimization of KCa2 Channel Activators as Neuroscience Tools and Potential DrugsR21NS072585 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2011 to 2012
$440k
CIHR NS072585NINDS NIH HHS R21 NS072585
6 · The paper itself

Abstract

aimsEndothelial SK(Ca) and IK(Ca) channels play an important role in the regulation of vascular function and systemic blood pressure. Based on our previous findings that small molecule activators of SK(Ca) and IK(Ca) channels (i.e. NS309 and SKA-31) can inhibit myogenic tone in isolated resistance arteries, we hypothesized that this class of compounds may induce effective vasodilation in an intact vascular bed, such as the coronary circulation. METHODS AND

resultsIn a Langendorff-perfused, beating rat heart preparation, acute bolus administrations of SKA-31 (0.01-5 µg) dose-dependently increased total coronary flow (25-30%) in both male and female hearts; these responses were associated with modest, secondary increases in left ventricular (LV) systolic pressure and heart rate. SKA-31 evoked responses in coronary flow, LV pressure, and heart rate were qualitatively comparable to acute responses evoked by bradykinin (1 µg) and adenosine (10 µg). In the presence of apamin and TRAM-34, selective blockers of SK(Ca) and IK(Ca) channels, respectively, SKA-31 and bradykinin-induced responses were largely inhibited, whereas the adenosine-induced changes were blocked by ∼40%; TRAM-34 alone produced less inhibition. Sodium nitroprusside (SNP, 0.2 μg bolus dose) evoked changes in coronary flow, LV pressure, and heart rate were similar to those induced by SKA-31, but were unaffected by apamin + TRAM-34. The NOS inhibitor L-NNA reduced bradykinin- and adenosine-evoked changes, but did not affect responses to either SKA-31 or SNP.

conclusionOur study demonstrates that SKA-31 can rapidly and reversibly induce dilation of the coronary circulation in intact functioning hearts under basal flow and contractility conditions.

Indexed as

AnimalsApaminBenzothiazolesCoronary CirculationDose-Response Relationship, DrugFemaleHeart RateMaleNitric Oxide Synthase Type IIINitroprussidePotassium Channels, Calcium-ActivatedPyrazolesRatsRats, Sprague-DawleySystoleApaminBenzothiazolesnaphtho(1,2-d)thiazol-2-ylamineNitric Oxide Synthase Type IIINitroprussidePotassium Channels, Calcium-ActivatedPyrazolesTRAM 34

Identifiers

PMID23118129
PMCPMC3543990
OpenAlexW2094957401

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.