Evidence map›Paper›PMID 17942071›Full record

ArticleBiochimica et biophysica acta2008

PKA-dependent activation of the vascular smooth muscle isoform of KATP channels by vasoactive intestinal polypeptide and its effect on relaxation of the mesenteric resistance artery.

Yang Yang, Yun Shi, Shouli Guo, Shuang Zhang, Ningren Cui, Weiwei Shi, Daling Zhu, Chun Jiang

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Rapid Characterization of the Functional and Pharmacological Consequences of Cantú Syndrome KThe Journal of pharmacology and experimental therapeutics · 2023
    Article
  4. Kir6.1 and SUR2B in Cantú syndrome.American journal of physiology. Cell physiology · 2022
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. K(ATP) channel action in vascular tone regulation: from genetics to diseases.Sheng li xue bao : [Acta physiologica Sinica] · 2012
    Review
  18. Article
  19. Article
  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

8 authors at 2 institutions in 2 countries.

Yang YangDepartment of Biology, Georgia State University, 24 Peachtree Center Avenue, Atlanta, Georgia 30302-4010, USA.
Yun Shi
Shouli Guo
Shuang Zhang
Ningren Cui
Weiwei Shi
Daling Zhu
Chun Jiang
Georgia State University · USHarbin Medical University · CN

Funding

Vascular KATP Channel Modulation in Hypercapnic AcidosisR01HL067890 · NHLBI · GEORGIA STATE UNIVERSITY · PI JIANG, CHUN · 2003 to 2006
$1.2M
NHLBI NIH HHS HL067890NHLBI NIH HHS R01 HL067890
6 · The paper itself

Abstract

Vasoactive intestinal polypeptide (VIP) is a potent vasodilator and has been successfully used to alleviate hypertension. Consistently, disruption of VIP gene in mice leads to hypertension. However, its downstream targets in the vascular regulation are still not well demonstrated. To test the hypothesis that the vascular smooth muscle isoform of KATP channels is a downstream target of the VIP signaling, we performed the studies on the Kir6.1/SUR2B channel expressed in HEK293 cells. We found that the channel was strongly activated by VIP. Through endogenous VIP receptors, the channel activation was reversible and dependent on VIP concentrations with the midpoint-activation concentration approximately 10 nM. The channel activation was voltage-independent and could be blocked by KATP channel blocker glibenclamide. In cell-attached patches, VIP augmented the channel open-state probability with modest suppression of the single channel conductance. The VIP-induced Kir6.1/SUR2B channel activation was blocked by PKA inhibitor RP-cAMP. Forskolin, an adenylyl cyclase activator, activated the channel similarly as VIP. The effect of VIP was further evident in the native tissues. In acutely dissociated mesenteric vascular smooth myocytes, VIP activated the KATP currents in a similar manner as in HEK293 cells. In endothelium-free mesenteric artery rings, VIP produced concentration-dependent vasorelaxation that was attenuated by glibenclamide. These results therefore indicate that the vascular isoform (Kir6.1/SUR2B) of KATP channels is a target of VIP. The channel activation relies on the PKA pathway and produces mesenteric arterial relaxation.

Indexed as

AnimalsATP-Binding Cassette TransportersCell LineCyclic AMP-Dependent Protein KinasesHumansIn Vitro TechniquesIon Channel GatingIsoenzymesKATP ChannelsMaleMesenteric ArteriesMuscle, Smooth, VascularMyocytes, Smooth MusclePotassium ChannelsPotassium Channels, Inwardly RectifyingRatsAbcc9 protein, mouseATP-Binding Cassette TransportersCyclic AMP-Dependent Protein KinasesIsoenzymesKATP ChannelsPotassium ChannelsPotassium Channels, Inwardly RectifyingReceptors, DrugSulfonylurea ReceptorsuK-ATP-1 potassium channelVasoactive Intestinal Peptide

Identifiers

PMID17942071
PMCPMC2245864
OpenAlexW2056805709

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.