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Study · Measured the body's own peptide · 1994

2 results

Endothelin-1 stimulates the in vitro release of neurohypophyseal hormones, but not corticotropin-releasing hormone, via ETA receptors.

Yasin S, Costa A, Navarra P, Pozzoli G, Kostoglou-Athanassiou I, Forsling M, Grossman A

Neuroendocrinology1 Dec 1994Cited by 17 (Europe PMC)

PMID7535387 (opens in a new tab)DOI10.1159/000126796 (opens in a new tab)PepBankPUB-07535387
Publisher pagePubMedAsk about this study
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study2

No result from this study comes from a test of the peptide.

Natural levels measured2

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01LabEndogenous levelEx vivo tissueMechanism

    In rat hypothalamic explants, endothelin-1 at 10 nmol/l stimulated release of the body's own oxytocin.

    In plain wordsIn rat brain tissue in a dish, endothelin-1 made the tissue release more of its own oxytocin.

    Peptide
    Oxytocin
    Outcome
    IncreaseOT release after endothelin-1 at 10 nmol/l
    Study

    ratn: not reported in source

    Rat hypothalamic explants
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    both vasopressin and oxytocin at 10 nmol/l (p < 0.01 and 0.05, respectively).
    1 context sentence
    Summary · context
    We have therefore used a previously validated rat hypothalamic explant system in order to investigate the possible modulation of the neurohypophyseal hormones vasopressin and oxytocin, and corticotropin-releasing hormone (CRH), by endothelin-1 (ET-1) and endothelin-3 (ET-3).

    This result measures the body's own Oxytocin. Nobody was given the peptide. It is not evidence about taking it.

  2. 02LabEndogenous levelEx vivo tissueMechanism

    In rat hypothalamic explants, the ETA receptor antagonist BQ-123 totally blocked the OT release induced by 10 nmol/l endothelin-1.

    In plain wordsIn rat brain tissue in a dish, a drug blocking the ETA receptor fully stopped the endothelin-1 rise in the tissue's own oxytocin release.

    Peptide
    Oxytocin
    Outcome
    DecreaseOT release after endothelin-1 with BQ-123
    Study

    ratn: not reported in source

    Rat hypothalamic explants
    Comparator
    Endothelin-1 alone
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    The release of vasopressin and oxytocin induced by 10 nmol/l ET-1 were both totally blocked by co-incubation with either 1 or 10 mumol/l of the specific ETA receptor subtype antagonist cyclo (D-Trp-D-Asp-Pro-D-Val-Leu) (BQ-123).
    1 context sentence
    Summary · context
    We have therefore used a previously validated rat hypothalamic explant system in order to investigate the possible modulation of the neurohypophyseal hormones vasopressin and oxytocin, and corticotropin-releasing hormone (CRH), by endothelin-1 (ET-1) and endothelin-3 (ET-3).

    This result measures the body's own Oxytocin. Nobody was given the peptide. It is not evidence about taking it.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    11 Oct 2026, 20:03 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:52 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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