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Related Experiment Videos

Heparin attenuates norepinephrine-induced venoconstriction

F I Hawari1, B E Shykoff, J L Izzo

  • 1Department of Medicine, State University of New York at Buffalo, USA.

Vascular Medicine (London, England)
|October 31, 1998
PubMed
Summary
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Heparin, even at low doses, effectively reversed norepinephrine-induced vein constriction. This suggests a potential shared mechanism with insulin for vein relaxation, possibly involving nitric oxide.

Area of Science:

  • Pharmacology
  • Vascular Physiology
  • Biochemistry

Background:

  • Norepinephrine causes vasoconstriction in peripheral veins.
  • Heparin and insulin are known to affect vascular tone.
  • The nitric oxide pathway plays a role in vasodilation.

Purpose of the Study:

  • To investigate the effect of heparin on norepinephrine-induced venoconstriction.
  • To explore potential shared mechanisms between heparin and insulin in regulating vascular tone.
  • To examine the role of the nitric oxide pathway in heparin's venorelaxant effect.

Main Methods:

  • Measurement of venous size using a linear variable differential transformer (LVDT).
  • Infusion of saline, norepinephrine, insulin, and graded doses of heparin with norepinephrine.

Related Experiment Videos

  • Administration of methylene blue to inhibit the nitric oxide cGMP cascade.

    • Main Results:

    • Heparin significantly reduced norepinephrine-induced venoconstriction (p < 0.01).
    • Heparin's venorelaxant effects were observed at concentrations as low as 0.05 U/min.
    • Maximal heparin-induced venorelaxation correlated with maximal insulin effect (r = 0.8, p < 0.01) and was not additive with insulin.
    • Methylene blue attenuated heparin-induced venorelaxation.

    Conclusions:

    • Heparin attenuates norepinephrine-induced venoconstriction at both physiologic and pharmacologic concentrations.
    • A common venorelaxation mechanism for heparin and insulin is suggested by the correlation and lack of additivity of their maximal effects.
    • The nitric oxide pathway is implicated in heparin's venorelaxant action.