Evidence map›Paper›PMID 23884142›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Adenosine inhibits renin release from juxtaglomerular cells via an A1 receptor-TRPC-mediated pathway.

M Cecilia Ortiz-Capisano, Douglas K Atchison, Pamela Harding, Robert D Lasley, William H Beierwaltes

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Adenosine AAmerican journal of physiology. Renal physiology · 2017
    Article
  9. Review
  10. 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.

M Cecilia Ortiz-CapisanoHenry Ford Hospital, Dept. of Medicine, Hypertension and Vascular Research Division, 7088 E&R Bldg., 2799 W. Grand Blvd., Detroit, MI 48202. wbeierw1@hfhs.org.
Douglas K Atchison
Pamela Harding
Robert D Lasley
William H Beierwaltes
Henry Ford Health System · USWayne State University · US

Funding

Tubuloglomerular Feedback Regulation by Carbon MonoxideP01HL090550 · NHLBI · HENRY FORD HEALTH SYSTEM · PI ORTIZ, PABLO A. · 2009 to 2013
$10.2M
NHLBI NIH HHS PPG 5PO-1HL-090550-03
6 · The paper itself

Abstract

Renin is synthesized and released from juxtaglomerular (JG) cells. Adenosine inhibits renin release via an adenosine A1 receptor (A1R) calcium-mediated pathway. How this occurs is unknown. In cardiomyocytes, adenosine increases intracellular calcium via transient receptor potential canonical (TRPC) channels. We hypothesized that adenosine inhibits renin release via A1R activation, opening TRPC channels. However, higher concentrations of adenosine may stimulate renin release through A2R activation. Using primary cultures of isolated mouse JG cells, immunolabeling demonstrated renin and A1R in JG cells, but not A2R subtypes, although RT-PCR indicated the presence of mRNA of both A2AR and A2BR. Incubating JG cells with increasing concentrations of adenosine decreased renin release. Different concentrations of the adenosine receptor agonist N-ethylcarboxamide adenosine (NECA) did not change renin. Activating A1R with 0.5 μM N6-cyclohexyladenosine (CHA) decreased basal renin release from 0.22 ± 0.05 to 0.14 ± 0.03 μg of angiotensin I generated per milliliter of sample per hour of incubation (AngI/ml/mg prot) (P < 0.03), and higher concentrations also inhibited renin. Reducing extracellular calcium with EGTA increased renin release (0.35 ± 0.08 μg AngI/ml/mg prot; P < 0.01), and blocked renin inhibition by CHA (0.28 ± 0.06 μg AngI/ml/mg prot; P < 0. 005 vs. CHA alone). The intracellular calcium chelator BAPTA-AM increased renin release by 55%, and blocked the inhibitory effect of CHA. Repeating these experiments in JG cells from A1R knockout mice using CHA or NECA demonstrated no effect on renin release. However, RT-PCR showed mRNA from TRPC isoforms 3 and 6 in isolated JG cells. Adding the TRPC blocker SKF-96365 reversed CHA-mediated inhibition of renin release. Thus A1R activation results in a calcium-dependent inhibition of renin release via TRPC-mediated calcium entry, but A2 receptors do not regulate renin release.

Indexed as

Renin InhibitorsAdenosineAngiotensin IIAnimalsFemaleJuxtaglomerular ApparatusKidney GlomerulusMaleMiceMice, Inbred C57BLMice, KnockoutReceptor, Adenosine A1ReninSignal TransductionTransient Receptor Potential ChannelsAdenosineAngiotensin IIReceptor, Adenosine A1ReninRenin InhibitorsTransient Receptor Potential ChannelsA1Radenosineadenosine receptorscalciumCHArenintransient receptor potential canonical

Identifiers

PMID23884142
PMCPMC3798729
OpenAlexW2076565467

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.