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Beta-adrenergic responsiveness is regulated selectively in hypertension
R D Feldman1, D J Freeman, G S Bierbrier
1Department of Medicine, University of Western Ontario, London, Canada.
Clinical Pharmacology and Therapeutics
|December 1, 1993
Summary
Hypertension impairs beta-adrenergic receptor function. Lowering blood pressure with verapamil or hydrochlorothiazide did not restore this vascular response, suggesting selective regulation in hypertension.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Beta-adrenergic receptor responsiveness is impaired in patients with hypertension.
- A low-sodium diet has been shown to correct this defect and lower blood pressure.
Purpose of the Study:
- To investigate if the upregulation of beta-adrenergic receptor function in hypertension is a nonspecific effect of lowering blood pressure.
- To assess vascular beta-adrenergic response after pharmacologic antihypertensive treatment.
Main Methods:
- Patients with hypertension underwent randomized treatments with placebo, verapamil, and hydrochlorothiazide.
- Vascular beta-adrenergic response was measured using dorsal hand vein linear differential transformer techniques.
- Measurements were taken after 2 weeks of treatment.
Main Results:
- Verapamil lowered blood pressure but did not significantly upregulate vascular beta-adrenergic response compared to placebo.
- Hydrochlorothiazide treatment did not significantly differ in vascular beta-adrenergic responsiveness compared to verapamil.
- Reduction of blood pressure with either drug did not correct the impaired beta-adrenergic responsiveness.
Conclusions:
- Pharmacologic reduction of blood pressure in hypertension with verapamil or hydrochlorothiazide does not correct the defect in vascular beta-adrenergic responsiveness.
- Vascular beta-adrenergic response in hypertension appears to be regulated selectively, not solely by blood pressure reduction.