Diltiazem versus propranolol in essential hypertension: Responses of rest and exercise blood pressure and effects on exercise capacity

Jadwiga Szlachcic, Alan T. Hirsch, Julio F. Tubau, Carol Vollmer, Steven Henderson, Barry M. Massie

Research output: Contribution to journalArticlepeer-review

32 Scopus citations

Abstract

Both β-blocking and calcium channel-blocking drugs are being used with increasing frequency as initial therapy for essential hypertension. The present study was designed to compare the antihypertensive effects of a β-blocking drug, propranolol, with a calcium channel-blocking drug, diltiazem, at rest and during upright bicycle exercise and to determine whether exercise capacity is altered by these therapies. Twenty-one patients with uncomplicated systemic hypertension and a diastolic blood pressure (BP) of 95 to 110 mm Hg without medication were randomly assigned to propranolol or diltiazem therapy in a double-blind manner. The total daily dosages were titrated as needed, from 160 to 480 mg of propranolol (mean 371 mg) and 120 to 360 mg of diltiazem (mean 307 mg) over 12 weeks, and the titrated dose was maintained for 4 additional weeks. Both drugs significantly reduced supine BP (from 149 ± 14/101 ± 4 to 136 ± 17 89 ± 10 mm Hg with propranolol and from 157 ± 14 103 ± 4 to 144 ± 13 93 ± 8 with diftiazem. Only diltiazem reduced BP during submaximal exercise, but both agents produced significant responses during maximal exercise. Diftiazem had no effect on maximal heart rate, exercise duration or O2 uptake, whereas propranolol reduced maximal VO2 from 27 ± 6 to 22 ± 6 ml/min/kg (p <0.01) and also shortened duration of exercise. Propranolol, despite its effects on heart rate, maintained the workload VO2 relation at submaximal loads, suggesting an increased, oxygen delivery. However, these adaptive mechanisms apppear to be insufficient during maximal effort.

Original languageEnglish (US)
Pages (from-to)393-399
Number of pages7
JournalThe American Journal of Cardiology
Volume59
Issue number5
DOIs
StatePublished - Feb 15 1987

Bibliographical note

Funding Information:
From the Cardiology Service of the San Francisco Veterans Administration Medical Center and the Department of Medicine and Cardiovascular Research Institute, University of California, San Francisco, California. This work was supported by the Veterans Administration Research Service, Washington, D.C.; Grants HL28146 and GM07546 from the National Institutes of Health, Bethesda, Maryland; and Marion Laboratories, Kansas City, Missouri. Manuscript received June 24, 1986; revised manuscript received August 15,1986, accepted August 18,1986. Address for reprints: Barry Massie, MD, Cardiology Division (lllC), Veterans Administration Medical Center, 4150 Clement Street, San Francisco, California 94121.

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