Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1983;67:1076-1084

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McLeod, A. A.
Right arrow Articles by Shand, D. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McLeod, A. A.
Right arrow Articles by Shand, D. G.

Circulation, Vol 67, 1076-1084, Copyright © 1983 by American Heart Association


ARTICLES

Differentiation of hemodynamic, humoral and metabolic responses to beta 1- and beta 2-adrenergic stimulation in man using atenolol and propranolol

AA McLeod, JE Brown, C Kuhn, BB Kitchell, FA Sedor, RS Williams and DG Shand

The respective contributions of beta-adrenoceptor subtypes to the hemodynamic, humoral and metabolic consequences of adrenergic stimulation during graded exercise in man were investigated using nonselective beta-adrenoceptor blockade with propranolol and beta 1- adrenoceptor blockade with atenolol. Doses of these agents that produced comparable suppression of beta 1 response as measured by antagonism of cardioacceleration during exercise were selected. Six healthy, nonsmoking males received these drugs in a placebo-controlled, Latin-square, randomized manner using a double-blind protocol. Both drugs produced comparable reductions of systolic blood pressure and elevation of diastolic blood pressure compared with placebo as exercise load increased. Propranolol produced higher peak epinephrine levels than atenolol or placebo (808 +/- 162, 640 +/- 190 and 584 +/- 153 pg/ml, respectively, p = 0.03), but norepinephrine levels did not show significant differences. Plasma renin activity was similarly suppressed both at rest and during all grades of exercise by both drugs. Lactate levels during moderate exercise were significantly lower after propranolol than after either atenolol or placebo (p = 0.03), but were similar at heavy work loads. Plasma glucose values rose on placebo (from 96.5 +/- 2.1 to 97.7 +/- 2.7 mg/dl) and on atenolol (from 99.7 +/- 2.2 to 102.1 +/- 4.8 mg/dl), but fell on propranolol (from 96.4 +/- 1.9 mg/dl to 87.2 +/- 2.5 mg/dl, p less than 0.01). These results indicate that blockade of vascular smooth muscle beta 2 receptors does not substantially alter hemodynamics during intense short-term exercise. Stimulation of renin release and lipolysis are produced through beta 1- adrenoceptor mechanisms, whereas beta 2 adrenoceptors are important in the provision of carbohydrate as an energy substrate for exercising muscle.


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
D. K. Rohrer, A. Chruscinski, E. H. Schauble, D. Bernstein, and B. K. Kobilka
Cardiovascular and Metabolic Alterations in Mice Lacking Both beta 1- and beta 2-Adrenergic Receptors
J. Biol. Chem., June 11, 1999; 274(24): 16701 - 16708.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
E. J. Eichhorn and M. R. Bristow
Medical Therapy Can Improve the Biological Properties of the Chronically Failing Heart: A New Era in the Treatment of Heart Failure
Circulation, November 1, 1996; 94(9): 2285 - 2296.
[Abstract] [Full Text]


Home page
ANGIOLOGYHome page
S. Krauss, E. Spitz, A. Krauss, B. Grizotzki, and S. Clement
Treatment of Hypertension in Mild Asthmatic Patients With Atenolol
Angiology, December 1, 1984; 35(12): 773 - 778.
[Abstract] [PDF]