Evidence map›Paper›PMID 11249849›Full record

ArticleAmerican journal of physiology. Renal physiology2001

Influence of Ca(2+)-activated K(+) channels on rat renal arteriolar responses to depolarizing agonists.

R W Fallet, J P Bast, K Fujiwara, N Ishii, S C Sansom, P K Carmines

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 45 citations in OpenAlex.

  1. CaMolecules (Basel, Switzerland) · 2023
    Review
  2. Article
  3. Article
  4. Article
  5. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  6. Review
  7. Smooth muscle contractile diversity in the control of regional circulations.American journal of physiology. Heart and circulatory physiology · 2014
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Complex interactions of NO/cGMP/PKG systems on Ca2+ signaling in afferent arteriolar vascular smooth muscle.American journal of physiology. Heart and circulatory physiology · 2010
    Article
  13. Article
  14. Article
  15. 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

6 authors at 1 institution in 1 country.

R W FalletDepartment of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575, USA.
J P Bast
K Fujiwara
N Ishii
S C Sansom
P K Carmines
University of Nebraska Medical Center · US

Funding

HORMONAL INFLUENCES ON THE RENAL MICROVASCULATURER01DK039202 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CARMINES, PAMELA K · 1992 to 2002
$531k
MICROVASCULAR CONTROL OF JUXTAMEDULLARY NEPHRON FUNCTIONR29DK039202 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CARMINES, PAMELA K · 1987 to 1989
–
NIDDK NIH HHS DK-39202NIDDK NIH HHS R01 DK039202
6 · The paper itself

Abstract

Experiments were performed to evaluate the hypothesis that opening of Ca(2+)-activated K(+) channels (BK(Ca) channels) promotes juxtamedullary arteriolar dilation and curtails constrictor responses to depolarizing agonists. Under baseline conditions, afferent and efferent arteriolar lumen diameters averaged 23.4 +/- 0.9 (n = 36) and 22.8 +/- 1.1 (n = 13) microm, respectively. The synthetic BK(Ca) channel opener NS-1619 evoked concentration-dependent afferent arteriolar dilation. BK(Ca) channel blockade (1 mM tetraethylammonium; TEA) decreased afferent diameter by 15 +/- 3% and prevented the dilator response to 30 microM NS-1619. ANG II (10 nM) decreased afferent arteriolar diameter by 44 +/- 4%, a response that was reduced by 30% during NS-1619 treatment; however, TEA failed to alter afferent constrictor responses to either ANG II or arginine vasopressin. Neither NS-1619 nor TEA altered agonist-induced constriction of the efferent arteriole. Thus, although the BK(Ca) channel agonist was able to curtail afferent (but not efferent) arteriolar constrictor responses to ANG II, BK(Ca) channel blockade did not allow exaggerated agonist-induced arteriolar constriction. These observations suggest that the BK(Ca) channels evident in afferent arteriolar smooth muscle do not provide a prominent physiological brake on agonist-induced constriction under our experimental conditions.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin IIAnimalsArteriolesBenzimidazolesCalciumEnalaprilatJuxtaglomerular ApparatusMaleMembrane PotentialsMuscle, Smooth, VascularPotassium ChannelsRatsRats, Sprague-DawleyRenal ArteryTetraethylammoniumAngiotensin-Converting Enzyme InhibitorsAngiotensin IIBenzimidazolesCalciumEnalaprilatNS 1619Potassium ChannelsTetraethylammoniumVasoconstrictor Agents

Identifiers

PMID11249849
PMCPMC2570964
OpenAlexW2136809503

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.