Evidence map›Paper›PMID 21153751›Full record

ArticleClinical and experimental nephrology2011

Effects of connexin-mimetic peptides on perfusion pressure in response to phenylephrine in isolated, perfused rat kidneys.

Honglan Piao, Ayako Sato, Yukiko Nozawa, Wei Sun, Tetsuo Morioka, Takashi Oite

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Article in Clinical and experimental nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Functional roles of connexins and pannexins in the kidney.Cellular and molecular life sciences : CMLS · 2015
    Review
  4. Article
  5. Exploring the mechanisms of renoprotection against progressive glomerulosclerosis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2011
    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 2 institutions in 1 country.

Honglan PiaoDepartment of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8510, Japan.
Ayako Sato
Yukiko Nozawa
Wei Sun
Tetsuo Morioka
Takashi Oite
Niigata University · JPNiigata University Medical and Dental Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGap junction intercellular communication plays a fundamental role in various tissues and organs. Gap junctions transfer ions and molecules between adjacent cells and are formed by connexins (Cx). It is supposed that vascular conducted responses, which most likely spread through gap junctions in vascular beds, regulate microcirculatory blood flow and maintain vascular resistance. This study provides functional evidence supporting the critical role of gap junctions in a physiological setting and in phenylephrine (PE)-induced vasoconstriction using an ex vivo kidney perfusion technique.

methodsUsing the isolated, perfused kidney model, infusion of gap junction inhibitors and PE, we examined the local effect of gap junction communication. Additionally, gap junction proteins Cx37, Cx40 and Cx43 were detected by immunofluorescence.

resultsFirst, changes in the perfusion pressure were analyzed by infusing the nonselective gap junction uncoupler, 18α-glycyrrhetinic acid (18α-GA), and specific connexin-mimetic peptide inhibitors, (37,43)Gap27, (40)Gap27 and (43)Gap26. Administration of 18α-GA and (43)Gap26 significantly elevated perfusion pressure while infusion of (40)Gap27 and (37,43)Gap27 had no effect. Second, we examined the effect of infusing gap junction inhibitors on PE-induced vasoconstriction. Infusion of 18α-GA and (40)Gap27 significantly suppressed the increase in perfusion pressure induced by PE, while (43)Gap26 and (37,43)Gap27 had no effect. Third, we confirmed by immunofluorescence that Cx37, Cx40 and Cx43 were found in the endothelial cells of interstitial microvessels and that Cx40 was localized in glomerular mesangial cells as well as in smooth muscle cells of the juxtaglomerular area.

conclusionsThis study showed that Cx43 plays a pivotal role in regulating renal vascular resistance and that Cx40 attenuates PE-induced vasoconstriction. These results provide new evidence that gap junctions may control renal circulation and vascular responses.

Indexed as

AnimalsConnexin 43ConnexinsGap Junction alpha-5 ProteinGap JunctionsGlycyrrhetinic AcidIn Vitro TechniquesMalePeptidesPerfusionPhenylephrineRatsRats, WistarRenal CirculationVasoconstriction18alpha-glycyrrhetinic acidConnexin 43ConnexinsGap Junction alpha-5 ProteinGlycyrrhetinic AcidPeptidesPhenylephrine

Identifiers

PMID21153751
OpenAlexW2025454158

What OpenQuestion holds

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Registered trials

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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.