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Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Nitric Oxide Signaling Pathway01:28

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Hormonal Regulation

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Related Experiment Video

Updated: May 25, 2026

Intracavernosal Pressure Recording to Evaluate Erectile Function in Rodents
08:03

Intracavernosal Pressure Recording to Evaluate Erectile Function in Rodents

Published on: June 6, 2018

Endogenous urotensin II selectively modulates erectile function through eNOS.

Roberta d'Emmanuele di Villa Bianca1, Emma Mitidieri, Ferdinando Fusco

  • 1Interdepartmental Research Centre for Sexual Medicine (CIRMS), University of Naples, Federico II, Naples, Italy.

Plos One
|February 10, 2012
PubMed
Summary
This summary is machine-generated.

Urotensin II (U-II) triggers penile erection by activating nitric oxide (NO) production in the human corpus cavernosum. This U-II/UT pathway presents a potential new therapeutic target for erectile dysfunction.

Related Experiment Videos

Last Updated: May 25, 2026

Intracavernosal Pressure Recording to Evaluate Erectile Function in Rodents
08:03

Intracavernosal Pressure Recording to Evaluate Erectile Function in Rodents

Published on: June 6, 2018

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Urology

Background:

  • Urotensin II (U-II) is a peptide hormone found in various species, including humans, acting via the UT receptor.
  • The U-II/UT pathway is implicated in human penile function, but its precise mechanism remains unclear.
  • Investigating U-II's role in penile erection is crucial for understanding erectile dysfunction.

Purpose of the Study:

  • To elucidate the molecular mechanisms of U-II-induced relaxation in the human corpus cavernosum.
  • To determine the relationship between the U-II/UT pathway and the L-arginine/Nitric Oxide (NO) pathway.

Main Methods:

  • Quantitative RT-PCR to confirm U-II expression in human corpus cavernosum.
  • Fluorometric analysis to measure NO production following U-II challenge.
  • Western blot analysis to assess eNOS phosphorylation.
  • Pharmacological modulation and co-immunoprecipitation studies to confirm pathway interactions.

Main Results:

  • U-II significantly increased NO production in human corpus cavernosum tissue.
  • U-II-induced relaxation was dependent on eNOS activation and phosphorylation.
  • Wortmannin and geldanamycin inhibited U-II-induced relaxation, confirming eNOS involvement.
  • UT receptor and eNOS were shown to co-immunoprecipitate, indicating a functional complex.

Conclusions:

  • Urotensin II is synthesized and released locally within the human corpus cavernosum.
  • The U-II/UT pathway mediates penile erection through the activation of endothelial nitric oxide synthase (eNOS).
  • The U-II/UT pathway represents a promising novel therapeutic target for treating erectile dysfunction.