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Related Experiment Videos

H2-receptor-mediated vasodilation contributes to postexercise hypotension.

Jennifer L McCord1, Julie M Beasley, John R Halliwill

  • 1Department of Human Physiology, 122 Esslinger Hall, 1240 University of Oregon, Eugene, Oregon 97403-1240, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|September 6, 2005
PubMed
Summary

Histamine H2-receptors contribute to postexercise hypotension by mediating vasodilation. Blocking these receptors with ranitidine significantly reduced exercise-induced vasodilation and hypotension in healthy adults.

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Area of Science:

  • Exercise Physiology
  • Cardiovascular Research
  • Pharmacology

Background:

  • Postexercise hypotension is a phenomenon characterized by reduced blood pressure following aerobic exercise.
  • Histamine H1-receptors are known to mediate vasodilation contributing to this response.
  • The role of histamine H2-receptors in postexercise hypotension remains less understood.

Purpose of the Study:

  • To investigate the potential contribution of histamine H2-receptor-mediated vasodilation to postexercise hypotension.
  • To determine if blocking H2-receptors affects the blood pressure and vascular conductance changes after exercise.

Main Methods:

  • Ten healthy participants completed a 60-minute cycling exercise at 60% peak oxygen uptake.
  • Measurements included arterial pressure, cardiac output, and femoral blood flow.

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  • Participants were studied on a control day and a day they received oral ranitidine (an H2-receptor antagonist).
  • Main Results:

    • On the control day, postexercise measurements showed significant increases in femoral and systemic vascular conductance and a reduction in mean arterial pressure.
    • With ranitidine, postexercise femoral and systemic vascular conductances were not elevated, and mean arterial pressure was not reduced.
    • Femoral and systemic vascular conductances were significantly lower, and mean arterial pressure was higher on the ranitidine day compared to the control day.

    Conclusions:

    • Histamine H2-receptor-mediated vasodilation plays a significant role in the early postexercise hypotension response.
    • Blocking H2-receptors with ranitidine blunts postexercise hypotension and reduces exercise-induced vasodilation.
    • These findings highlight the importance of the histamine system in cardiovascular regulation after exercise.