Circulation, Vol 67, 1076-1084, Copyright © 1983 by American Heart Association
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.
ARTICLES
Differentiation of hemodynamic, humoral and metabolic responses to beta 1- and beta 2-adrenergic stimulation in man using atenolol and propranolol
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