Evidence map›Paper›PMID 15804979›Full record

ReviewMicrocirculation (New York, N.Y. : 1994)

Potassium channels in the peripheral microcirculation.

William F Jackson

Open access · greenAbstract readReview
In one paragraph

Review in Microcirculation (New York, N.Y. : 1994). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

141 citing papers in PubMed, 335 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. KMicrovascular research · 2025
    Article
  9. Article
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  11. Pharmaceuticals (Basel, Switzerland) · 2024
    Article
  12. Article
  13. Role of KCardiovascular therapeutics · 2023
    Article
  14. KMicrocirculation (New York, N.Y. : 1994) · 2023
    Article
  15. Novel Thioxothiazolo[3,4-ACS medicinal chemistry letters · 2022
    Article
  16. Boldine, an Alkaloid fromEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. Review

81 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

William F JacksonDepartment of Biological Sciences, Western Michigan University, Kalamazoo, MI 49008-5410, USA. william.jackson@wmich.edu
Western Michigan University · US

Funding

CONTROL OF MICROVASCULAR FUNCTION BY OXYGENR01HL032469 · NHLBI · WESTERN MICHIGAN UNIVERSITY · PI JACKSON, WILLIAM F. · 1987 to 2006
$1.1M
CONTROL OF MICROVASCULAR FUNCTION BY OXYGENR23HL032469 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI JACKSON, WILLIAM F. · 1985 to 1986
–
NHLBI NIH HHS HL 32469NHLBI NIH HHS R01 HL032469
6 · The paper itself

Abstract

Vascular smooth muscle (VSM) cells, endothelial cells (EC), and pericytes that form the walls of vessels in the microcirculation express a diverse array of ion channels that play an important role in the function of these cells and the microcirculation in both health and disease. This brief review focuses on the K+ channels expressed in smooth muscle and endothelial cells in arterioles. Microvascular VSM cells express at least four different classes of K+ channels, including inward-rectifier K+ channels (Kin), ATP-sensitive K+ channels (KATP), voltage-gated K+ channels (Kv), and large conductance Ca2+-activated K+ channels (BKCa). VSM KIR participate in dilation induced by elevated extracellular K+ and may also be activated by C-type natriuretic peptide, a putative endothelium-derived hyperpolarizing factor (EDHF). Vasodilators acting through cAMP or cGMP signaling pathways in VSM may open KATP, Kv, and BKCa, causing membrane hyperpolarization and vasodilation. VSMBKc. may also be activated by epoxides of arachidonic acid (EETs) identified as EDHF in some systems. Conversely, vasoconstrictors may close KATP, Kv, and BKCa through protein kinase C, Rho-kinase, or c-Src pathways and contribute to VSM depolarization and vasoconstriction. At the same time Kv and BKCa act in a negative feedback manner to limit depolarization and prevent vasospasm. Microvascular EC express at least 5 classes of K+ channels, including small (sKCa) and intermediate(IKCa) conductance Ca2+-activated K+ channels, Kin, KATP, and Kv. Both sK and IK are opened by endothelium-dependent vasodilators that increase EC intracellular Ca2+ to cause membrane hyper-polarization that may be conducted through myoendothelial gap junctions to hyperpolarize and relax arteriolar VSM. KIR may serve to amplify sKCa- and IKCa-induced hyperpolarization and allow active transmission of hyperpolarization along EC through gap junctions. EC KIR channels may also be opened by elevated extracellular K+ and participate in K+-induced vasodilation. EC KATP channels may be activated by vasodilators as in VSM. Kv channels may provide a negative feedback mechanism to limit depolarization in some endothelial cells.

Indexed as

AnimalsEndothelium, VascularHumansMicrocirculationMuscle, Smooth, VascularPotassium ChannelsPotassium Channels

Identifiers

PMID15804979
PMCPMC1405752
OpenAlexW2021739695

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.