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Related Experiment Videos

Adjacent bronchus attenuates pulmonary arterial contractility.

Satyan Lakshminrusimha1, James A Russell, Sylvia F Gugino

  • 1Department of Pediatrics, State University of New York at Buffalo, Center for Developmental Biology of the Lung, USA. slakshmi@buffalo.edu

American Journal of Physiology. Lung Cellular and Molecular Physiology
|April 4, 2006
PubMed
Summary

Bronchus-derived relaxing factor (BrDRF) reduces pulmonary artery contractility by stimulating nitric oxide (NO) production. This factor can cross the adventitia, suggesting a novel pathway for regulating vascular tone.

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Area of Science:

  • Pulmonary vascular physiology
  • Nitric oxide signaling

Background:

  • Bronchus-derived relaxing factor (BrDRF) is known to decrease pulmonary artery (PA) contractility via nitric oxide (NO) synthesis.
  • The adventitia layer of PAs is typically considered a barrier to NO diffusion.

Purpose of the Study:

  • To investigate the effect of an adjacent bronchus on PA contractility to norepinephrine in lambs.
  • To determine if BrDRF can influence PA contractility from the adventitial side.
  • To elucidate the role of NO pathway inhibitors, cytochrome P-450, nerve activity, and superoxide in BrDRF-mediated relaxation.

Main Methods:

  • Studied PA rings with and without attached bronchi in juvenile lambs.
  • Utilized inhibitors of the NO pathway, cytochrome P-450, nerve activity, and a superoxide scavenger.

Related Experiment Videos

  • Exposed adventitial and endothelial sides of dissected PAs to an unattached bronchus in a sided chamber.

    • Main Results:

    • The presence of an attached bronchus significantly reduced norepinephrine-induced PA contractions.
    • This inhibitory effect was reversed by NO pathway inhibitors and disruption of bronchial epithelium.
    • An unattached bronchus effectively inhibited PA contractility when applied to the adventitial side.

    Conclusions:

    • BrDRF is a diffusible factor that can cross the PA adventitia.
    • BrDRF likely stimulates NO production within the pulmonary artery wall.
    • This mechanism suggests a novel way BrDRF influences pulmonary vascular tone.