title: Mechanism of antihypertensive action of dilevalol compared with that of "cardioselective" beta-blocking agents.
abstract: The hemodynamic effects of dilevalol, a nonselective beta-adrenergic blocking agent with vasodilating properties, were evaluated in 34 hypertensive patients and compared with those of the "cardioselective" beta blockers atenolol and metoprolol in 21 patients. Hemodynamic measurements were obtained at baseline, after acute treatment (first dose) with dilevalol (400 mg) and atenolol (50 mg) or metoprolol (100 mg), and again after subchronic treatment with these agents. After both acute and subchronic treatment (mean daily dose 1,042 mg), dilevalol significantly reduced mean arterial pressure (MAP, p less than 0.0001), by significantly reducing systemic vascular resistance index (SVRI, p less than 0.001), and by not significantly altering cardiac index (CI). In contrast, atenolol and metoprolol significantly reduced MAP (p less than 0.002) by significantly reducing CI (p less than 0.0001), with a concomitant increase in SVRI (p less than 0.007). Heart rate (HR) was reduced significantly less (p less than 0.006) with dilevalol than with the cardioselective agents. Correlation of the decrease in MAP with other hemodynamic parameters revealed that the effects on MAP of acute treatment with the cardioselective drugs are related to a decrease in HR (r = 0.63, p = 0.002), whereas those of subchronic treatment are correlated to a decrease in CI (r = 0.59, p = 0.01). The decrease in MAP after acute and subchronic dilevalol treatment is correlated primarily with SVRI (r = 0.46 to 0.49, p less than 0.01) and only secondarily with HR (r = 0.34, p less than 0.05). Therefore, the main mechanism of antihypertensive action for dilevalol is vasodilation, in contrast to the cardioselective agents, which is beta blockade.
authors.affiliation: Division of Cardiology, Jack D. Weiler Hospital of the Albert Einstein College of Medicine, Bronx, New York 10461.
authors.forename: J A
authors.initials: JA
authors.lastname: Strom
authors.forename: D G
authors.initials: DG
authors.lastname: Vidt
authors.forename: W
authors.initials: W
authors.lastname: Bugni
authors.forename: J
authors.initials: J
authors.lastname: Atkins
authors.forename: F
authors.initials: F
authors.lastname: Fouad-Tarazi
authors.forename: J
authors.initials: J
authors.lastname: Cubbon
authors.forename: M P
authors.initials: MP
authors.lastname: Poland
mesh_terms: D000328:Adult; D000368:Aged; D001262:Atenolol / Q000494:pharmacology*; D005260:Female; D006321:Heart / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D007741:Labetalol / Q000494:pharmacology*; D008297:Male; D008790:Metoprolol / Q000494:pharmacology*; D008875:Middle Aged; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D001262:Atenolol; D008790:Metoprolol; D007741:Labetalol