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H1 receptor-mediated vasodilatation contributes to postexercise hypotension.
Jennifer M Lockwood1, Brad W Wilkins, John R Halliwill
1Department of Human Physiology, University of Oregon, Eugene, OR 97403-1240 USA.
The Journal of Physiology
|December 25, 2004
Summary
Histamine H1 receptors contribute to postexercise hypotension by causing peripheral vasodilation after aerobic exercise. Blocking these receptors with fexofenadine reduced vasodilation and hypotension.
Area of Science:
- Exercise Physiology
- Cardiovascular Physiology
- Pharmacology
Background:
- Postexercise hypotension in healthy individuals is linked to unexplained peripheral vasodilation.
- Histamine release during exercise may cause vasodilation via H1 receptors.
Purpose of the Study:
- To investigate the role of H1 receptor-mediated vasodilation in postexercise hypotension.
- To determine if blocking H1 receptors affects blood pressure and vascular conductance after exercise.
Main Methods:
- 14 healthy men and women cycled for 60 minutes at 60% intensity.
- Participants were randomized to receive either a control or an H1 receptor antagonist (fexofenadine).
- Arterial blood pressure and femoral blood flow were measured before and up to 90 minutes post-exercise.
Main Results:
- On the control day, femoral vascular conductance increased and mean arterial pressure decreased post-exercise.
- On the fexofenadine day, post-exercise femoral vascular conductance and mean arterial pressure remained unchanged.
- Fexofenadine did not affect pre-exercise hemodynamics.
Conclusions:
- H1 receptor-mediated vasodilation significantly contributes to postexercise hypotension.
- Blocking H1 receptors blunts exercise-induced vasodilation and hypotension.
- Histamine acting on H1 receptors is a key mechanism in postexercise hemodynamic regulation.