Effects of atenolol and hydrochlorothiazide on blood pressure and plasma catecholamines in essential hypertension
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Atenolol and hydrochlorothiazide effectively lower blood pressure in hypertensive patients. Hyperadrenergic individuals showed a greater blood pressure response to atenolol, indicating sympathetic nervous system activity influences treatment outcomes.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Background:
- Essential hypertension is a common condition requiring effective antihypertensive therapies.
- Understanding the role of the sympathetic nervous system in blood pressure regulation is crucial for optimizing treatment.
- Atenolol and hydrochlorothiazide are established antihypertensive medications with different mechanisms of action.
Purpose of the Study:
- To compare the antihypertensive effects of atenolol and hydrochlorothiazide against a placebo.
- To investigate the relationship between sympathetic nervous system activity and the blood pressure response to these drugs.
- To determine if "adrenergic status" predicts treatment efficacy.
Main Methods:
- A randomized, double-blind, crossover study involving 12 patients with essential hypertension.
- Patients received single daily doses of atenolol (100 mg), hydrochlorothiazide (50 mg), and placebo for 6 weeks each.
- Supine plasma norepinephrine levels were measured as an index of sympathetic activity to define "adrenergic status".
Main Results:
- Both atenolol and hydrochlorothiazide significantly reduced supine, standing, and post-exercise blood pressure compared to placebo (p < 0.01).
- Patients categorized as "hyperadrenergic" (high resting norepinephrine) showed a significantly greater blood pressure decrease with atenolol (-30/-20 mm Hg) compared to non-hyperadrenergic patients (-9/-11 mm Hg).
- Resting plasma norepinephrine levels did not predict the blood pressure response to hydrochlorothiazide, and "adrenergic status" remained relatively constant across treatment phases.
Conclusions:
- Atenolol and hydrochlorothiazide are effective antihypertensive agents, comparable in potency.
- Sympathetic nervous system activity, as indicated by "adrenergic status," appears to influence the blood pressure response to atenolol but not hydrochlorothiazide.
- Individual "adrenergic status" may be a useful predictor for atenolol therapy in essential hypertension.
Abstract:
The antihypertensive effects of atenolol and hydrochlorothiazide were compared with placebo in a randomized, double-blind crossover study, with the blood pressure responses related to sympathetic nervous system activity. Twelve patients with essential hypertension were given atenolol (100 mg), hydrochlorothiazide (50 mg), and placebo as single daily doses, each for 6 weeks. Mean supine, standing, and post-exercise blood pressures (mm Hg) on atenolol (155/94, 152/95, 177/93, respectively) and hydrochlorothiazide (154/99, 150/103, 172/96) were lower (p less than 0.01) than corresponding placebo values (172/109, 166/113, 204/111) at 6 weeks. The role of the sympathetic nervous system in the antihypertensive actions of atenolol and hydrochlorothiazide was examined. The supine plasma norepinephrine on placebo was used as an index of sympathetic activity to categorize each patient's "adrenergic status." The six "hyperadrenergic" patients with high resting norepinephrine values (mean, 302 pg/ml) exhibited a greater (p = 0.05) decrease in BP (-30/-20 mm Hg) on atenolol compared with the BP fall of -9/-11 mm Hg observed in the lower norepinephrine group (mean, 211 pg/ml). Resting plasma norepinephrine values did not predict the BP fall on hydrochlorothiazide. The "adrenergic status" of each patient as measured by the plasma norepinephrine concentration tended to be relatively constant regardless of therapy or the state of activity. In this study, atenolol was an effective antihypertensive agent comparable to hydrochlorothiazide in potency. Adrenergic status tended to predict the BP response to atenolol and was a relatively constant feature of the patients in all treatment phases.