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Clinical Trial
. 1982 Jan;71(2):129-37.

[The effect of beta-receptor antagonists and diuretics and their combination on blood pressure and pressure-rate product during ergometric work in hypertensive patients (author's transl)]

[Article in German]
  • PMID: 7072313
Clinical Trial

[The effect of beta-receptor antagonists and diuretics and their combination on blood pressure and pressure-rate product during ergometric work in hypertensive patients (author's transl)]

[Article in German]
I W Franz. Z Kardiol. 1982 Jan.

Abstract

1. Hypertensive patients are particularly endangered by disproportionately high increases in blood pressure during daily physical and emotional activity. For this reason, antihypertensive drugs should also be able to influence there pressure changes. 2. Therefore the ability of the beta-receptor antagonist acebutolol (400 mg/die) and of the diuretic mefrusid (25 mg/die) to reduce exercise-induced increases in blood pressure and pressure-rate product during and after standardized ergometric work (50--100 watts) was compared in a within-patient study of 42 outpatients with arterial hypertension (stage 1 to 2, WHO) aged 18 to 50 years. 3. Both drugs resulted in a significant reduction of systolic (p less than 0.05-p less than 0.001) and diastolic (p less than 0.05-p less than 0.001) blood pressure at rest. However, systolic and diastolic blood pressure (p less than 0.001) and pressure-rate product (p less than 0.001) during exercise were only significantly reduced by acebutolol. 4. The strongest blood pressure lowering effect under all conditions could be proven for the free and fixed combination of acebutolol and mefrusid. 5. From these findings it is concluded: (1) beta-adreno-receptor blocking agents are the drugs of first choice in the baseline therapy of mild to moderate arterial hypertension, (2) diuretic drugs potentiate the antihypertensive effect of beta-blocking agents. 6. This therapeutic regimen is recommended especially for hypertensives with ischemic heart disease, because diuretics fail to reduce pressure-rate product as a measure of myocardial O2-consumption.

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