Evidence map›Paper›PMID 8383697›Full record

ArticleThe Journal of clinical investigation1993

Involvement of endothelium-derived relaxing factor in the pressure control of renin secretion from isolated perfused kidney.

H Scholz, A Kurtz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

16 citing papers in PubMed, 90 citations in OpenAlex.

  1. Trial
  2. Review
  3. Regulation of renin secretion by renal juxtaglomerular cells.Pflugers Archiv : European journal of physiology · 2013
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Stimulation of renin secretion by nitric oxide is mediated by phosphodiesterase 3.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  9. Article
  10. Article
  11. Nitric oxide.Annals of the rheumatic diseases · 1996
    Review
  12. Tonic stimulation of renin gene expression by nitric oxide is counteracted by tonic inhibition through angiotensin II.Proceedings of the National Academy of Sciences of the United States of America · 1995
    Article
  13. Article
  14. Article
  15. Role of calcium ions in the pressure control of renin secretion from the kidneys.Pflugers Archiv : European journal of physiology · 1994
    Article
  16. 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

2 authors at 1 institution in 1 country.

H ScholzInstitut für Physiologie, Universität Regensburg, Germany.
A Kurtz
University of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Using isolated rat kidneys perfused at controlled pressure, we examined a potential role of endothelium-derived relaxing factor (EDRF) in the pressure control of renin secretion. We found that stimulation of EDRF release by acetylcholine (1 mumol/liter) increased mean perfusate flow rates from 15.0 +/- 0.5 to 18.0 +/- 0.5 ml/min per g and average renin secretion rates from 3.5 +/- 0.5 to 16.0 +/- 2.0 ng angiotensin I/h per min per g at a perfusion pressure of 100 mmHg (mean +/- SEM, n = 6). Those effects of acetylcholine were significantly reduced during inhibition of EDRF formation with NG-nitro-L-arginine (100 mumol/liter), but they were not affected with the cyclooxygenase inhibitor indomethacin (10 mumol/liter). Lowering of the perfusion pressure from 100 mmHg to 40 mmHg resulted in an increase of average renin secretion rates from 3.5 +/- 0.5 to 79 +/- 12 ng AngI/h per min per g under control conditions (n = 8), and to 171 +/- 20 ng AngI/h per min per g in the presence of 10 mumol/liter acetylcholine (n = 3). The rise of renin secretion in response to a reduction of the renal artery pressure was markedly attenuated with inhibitors of EDRF formation such as NG-nitro-L-arginine (100 mumol/liter) and related compounds. During inhibition of EDRF formation, addition of sodium nitroprusside (10 mumol/liter) increased mean perfusate flow rates from 12.0 +/- 0.5 to 23.0 +/- 2.0 ml/min per g and average renin secretion rates from 2.0 +/- 0.5 to 18.0 +/- 1.5 ng AngI/h per min per g at 100 mmHg (n = 5). Lowering of the perfusion pressure from 100 mmHg to 40 mmHg under those conditions increased average renin secretion rates to 220 +/- 14 ng AngI/h per min per g (n = 5). Taken together, our findings suggest that EDRF and related activators of soluble guanylate cyclase stimulate renin secretion from isolated kidneys, predominantly at lower perfusion pressure. Moreover, pressure control of renin secretion appears to require the tonical stimulation by intrarenal EDRF.

Indexed as

AcetylcholineAngiotensin IAnimalsArginineAtrial Natriuretic FactorCyclic GMPDiuresisIn Vitro TechniquesIsoproterenolKidneyMaleNG-Nitroarginine Methyl EsterNitric OxideNitroarginineNitroprussideomega-N-Methylarginine8-bromocyclic GMPAcetylcholineAngiotensin IArginineAtrial Natriuretic FactorCyclic GMPIsoproterenolNG-Nitroarginine Methyl EsterNitric OxideNitroarginineNitroprussideomega-N-MethylarginineRenin

Identifiers

PMID8383697
PMCPMC288063
OpenAlexW2016984858

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.