Evidence map›Paper›PMID 18604236›Full record

ArticleBritish journal of pharmacology2008

Smooth muscle alpha1D-adrenoceptors mediate phenylephrine-induced vasoconstriction and increases in endothelial cell Ca2+ in hamster cremaster arterioles.

W F Jackson, E M Boerman, E J Lange, S S Lundback, K D Cohen

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

45 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Cracking the Endothelial Calcium (CaInternational journal of molecular sciences · 2023
    Review
  6. Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems.American journal of physiology. Heart and circulatory physiology · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Voltage-gated CaAmerican journal of physiology. Heart and circulatory physiology · 2018
    Article
  15. Article
  16. Article
  17. AlphaPhysiological reports · 2018
    Article
  18. Article
  19. Article
  20. Regional heterogeneity in the mechanisms of myogenic tone in hamster arterioles.American journal of physiology. Heart and circulatory physiology · 2017
    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

5 authors at 2 institutions in 1 country.

W F JacksonDepartment of Pharmacology & Toxicology, Michigan State University, East Lansing, MI 48824, USA. jacks783@msu.edu
E M Boerman
E J Lange
S S Lundback
K D Cohen
Michigan State University · USKennedy Space Center · 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

background and purposealpha(1)-Adrenoceptor agonists induce Ca(2+)-transients in endothelial cells (ECs) of arterioles. However, the presence of alpha(1)-adrenoceptors on arteriolar ECs has not been excluded, and the identity of alpha(1)-adrenoceptor subtypes in arterioles only has been inferred from pharmacology. Therefore, we determined which subtypes were expressed by vascular smooth muscle cells (VSMCs) and ECs, and which subtype mediated alpha(1)-adrenoceptor-induced constriction. EXPERIMENTAL APPROACH: EC Ca(2+)-transients in isolated, cannulated hamster cremasteric arterioles or freshly isolated ECs were studied using Fura 2. Arteriolar diameter was measured by video microscopy. alpha(1)-Adrenoceptor expression was assessed by western blot of whole-arteriolar homogenates and real-time RT-PCR on enzymatically isolated VSMCs and ECs. KEY

resultsPhenylephrine-induced constriction and EC Ca(2+)-transients were abolished by the alpha(1)-adrenoceptor antagonist prazosin (30 nM) in arterioles. Phenylephrine-induced constriction was inhibited by the alpha(1D)-adrenoceptor antagonist BMY 7378 (K(B)=2.96 nM) and the alpha(1A)-adrenoceptor antagonist 5-methylurapidil (K(B)=4.08 nM), suggesting a significant role for alpha(1D)-adrenoceptors. Western blots confirmed alpha(1D)-adrenoceptor expression, but did not detect alpha(1A)-adrenoceptors. VSMCs expressed alpha(1D)- and alpha(1A)-, but not alpha(1B)-, adrenoceptor transcripts. No alpha(1)-adrenoceptor transcripts were detected in ECs. Neither phenylephrine (10 microM) nor noradrenaline (0.1-1 microM) elicited Ca(2+)-transients in freshly isolated ECs, whereas the endothelium-dependent vasodilators methacholine (1 microM) and substance P (100 nM) consistently increased Ca(2+). CONCLUSIONS AND IMPLICATIONS: We reject the hypothesis that hamster cremasteric arteriolar ECs express alpha(1)-adrenoceptors and conclude that alpha(1)-adrenoceptor agonists predominantly act on VSMC alpha(1D)-adrenoceptors to cause vasoconstriction and a subsequent rise in EC Ca(2+).

Indexed as

Adrenergic alpha-1 Receptor AgonistsAdrenergic alpha-AgonistsAnimalsArteriolesBlotting, WesternCalciumCricetinaeEndothelial CellsGene ExpressionMaleMuscle, Smooth, VascularPhenylephrineReceptors, Adrenergic, alpha-1Reverse Transcriptase Polymerase Chain ReactionVasoconstrictionVasoconstrictor AgentsAdrenergic alpha-1 Receptor AgonistsAdrenergic alpha-AgonistsCalciumPhenylephrineReceptors, Adrenergic, alpha-1Vasoconstrictor Agents

Identifiers

PMID18604236
PMCPMC2579662
OpenAlexW2039694740

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.