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Research Article Free access | 10.1172/JCI107237
Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220
Department of Pharmacology, University of Colorado Medical Center, Denver, Colorado 80220
Find articles by Bodem, G. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220
Department of Pharmacology, University of Colorado Medical Center, Denver, Colorado 80220
Find articles by Brammell, H. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220
Department of Pharmacology, University of Colorado Medical Center, Denver, Colorado 80220
Find articles by Weil, J. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80220
Department of Pharmacology, University of Colorado Medical Center, Denver, Colorado 80220
Find articles by Chidsey, C. in: JCI | PubMed | Google Scholar
Published April 1, 1973 - More info
The pharmacodynamic activities of two beta adrenergic antagonists, propranolol and practolol, were compared in eight hypertensive patients. The activity of each antagonist was established in relation to its blood concentration at maximal and submaximal adrenergic blockade defined by inhibition of exercise tachycardia. Maximal inhibition of exercise tachycardia was comparable with both drugs and averaged 74±7% of the control value during drug treatment. This inhibition was achieved with a blood concentration of 2.5±0.4 μg/ml practolol and 0.10±0.08 μg/ml propranolol. The antagonist activities of these drugs against adrenergic stimulation with isoproterenol infusion indicated a much greater relative potency of propranolol against this stimulus, and in vivo estimates of PA2 values differed by more than 600-fold. Relative antagonist activity of practolol during isoproterenol stimulation was equivalent both at cardiac (inotropic and chronotropic) and at vascular adrenergic receptors, whereas greater antagonist activity of propranolol was observed at vascular receptors than at cardiac receptors. Thus, the activity of practolol was not limited to cardiac receptors as previously suggested. Practolol did not reduce cardiac output at any dose level and the effect on resting blood pressure was small. Both practolol and propranolol had much greater hypotensive activity during exercise. These studies have defined the differing pharmacodynamic activities on the cardiovascular system of two effective beta adrenergic receptor antagonists and have established the blood levels of these antagonists necessary to achieve effective adrenergic blockade.