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Endogenous endothelin-1 limits exercise-induced vasodilation in hypertensive humans
Carmel M McEniery1, Ian B Wilkinson, David G Jenkins
1Clinical Pharmacology Unit and Research Centre, University of Endinburgh, Western General Hospital, United Kingdom. cmm41@cam.ac.uk
Hypertension (Dallas, Tex. : 1979)
|August 3, 2002
Summary
Essential hypertension impairs exercise vasodilation due to endothelin A (ET(A)) receptor activity. Blocking these receptors improved blood flow responses in hypertensive patients, suggesting a new treatment approach.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Essential hypertension is linked to increased endothelin-1 vasoconstriction.
- This may explain reduced vasodilation during exercise in hypertensive individuals.
Purpose of the Study:
- To investigate the impact of endothelin A (ET(A)) receptor blockade on exercise-induced vasodilation in hypertension.
- To determine if ET(A) receptor activity contributes to impaired vascular resistance reduction during exercise.
Main Methods:
- Assessed forearm blood flow responses to handgrip exercise at varying intensities in hypertensive and normotensive subjects.
- Administered intra-arterial infusions of an ET(A) receptor antagonist (BQ-123), hydralazine, and placebo.
- Compared responses before and after infusions.
Main Results:
- Hypertensive patients showed attenuated vasodilation during exercise compared to normotensive controls.
- Neither hydralazine nor placebo altered exercise vasodilation.
- BQ-123 significantly enhanced exercise vasodilation in hypertensives at higher workloads, but not in normotensives.
Conclusions:
- Impaired exercise vasodilation in essential hypertension is partly due to endogenous ET(A) receptor-mediated vasoconstriction.
- Endothelin receptor antagonists may improve exercise capacity in hypertensive patients.