Evidence map›Paper›PMID 9294131›Full record

ArticleThe Journal of clinical investigation1997

Novel autocrine feedback control of catecholamine release. A discrete chromogranin a fragment is a noncompetitive nicotinic cholinergic antagonist.

S K Mahata, D T O'Connor, M Mahata, S H Yoo, L Taupenot, H Wu, B M Gill, R J Parmer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

161 citing papers in PubMed, 1 synthesis or guideline pooled it, 392 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Direct vasoactive effects of the chromogranin A (CHGA) peptide catestatin in humans in vivo.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2010
    Trial
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  8. The role of chromogranin A cleavage products in onset of type 1 and 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026
    Review
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  14. Article
  15. Review
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101 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

S K MahataDepartment of Medicine and Center for Molecular Genetics, University of California, San Diego, California 92093, USA.
D T O'Connor
M Mahata
S H Yoo
L Taupenot
H Wu
B M Gill
R J Parmer
University of California, San Diego · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Catecholamine secretory vesicle core proteins (chromogranins) contain an activity that inhibits catecholamine release, but the identity of the responsible peptide has been elusive. Size-fractionated chromogranins antagonized nicotinic cholinergic-stimulated catecholamine secretion; the inhibitor was enriched in processed chromogranin fragments, and was liberated from purified chromogranin A. Of 15 synthetic peptides spanning approximately 80% of chromogranin A, one (bovine chromogranin A344-364 [RSMRLSFRARGYGFRGPGLQL], or catestatin) was a potent, dose-dependent (IC50 approximately 200 nM), reversible secretory inhibitor on pheochromocytoma and adrenal chromaffin cells, as well as noradrenergic neurites. An antibody directed against this peptide blocked the inhibitory effect of chromogranin A proteolytic fragments on nicotinic-stimulated catecholamine secretion. This region of chromogranin A is extensively processed within chromaffin vesicles in vivo. The inhibitory effect was specific for nicotinic cholinergic stimulation of catecholamine release, and was shared by this chromogranin A region from several species. Nicotinic cationic (Na+, Ca2+) signal transduction was specifically disrupted by catestatin. Even high-dose nicotine failed to overcome the inhibition, suggesting noncompetitive nicotinic antagonism. This small domain within chromogranin A may contribute to a novel, autocrine, homeostatic (negative-feedback) mechanism controlling catecholamine release from chromaffin cells and neurons.

Indexed as

Amino Acid SequenceAnimalsAntibodies, BlockingAutocrine CommunicationBarium CompoundsCalcimycinCalciumCattleChloridesChloroquineChromaffin CellsChromogranin AChromograninsDose-Response Relationship, DrugHomeostasisHumansAntibodies, Blockingbarium chlorideBarium CompoundsCalcimycinCalciumCHGA protein, humanChloridesChloroquineChromogranin Achromogranin A (344-364)chromogranin A, ratChromograninsN(alpha)-(N(alpha)-(N(alpha)-(tert-butyloxycarbonyl)glutaminyl)-N(1)-formyl-tryptophyl)phenylalanine benzyl esterNicotineNicotinic AntagonistsNorepinephrineOligopeptidesPeptide FragmentsPotassium ChlorideReceptors, Purinergic P2SodiumSubstance P

Identifiers

PMID9294131
PMCPMC508344
OpenAlexW2003049002

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.