Effects of β adrenergic blockade on plasma catecholamines in exercise

Irving, M. H.; Britton, B. J.; Wood, W. G.; Padgham, C.; Carruthers, Malcolm

doi:10.1038/248531a0

Cited by 103 publications

(33 citation statements)

References 8 publications

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“…Propranolol has been shown to be beneficial in experimental coronary occlusion (7) and in human myocardial infarction for a selected patient group (8)(9)(10). Recent studies have demonstrated, however, that propranolol increased plasma catecholamine contents in several clinical conditions (11)(12)(13), and thus caused concern about its use in acute myocardial infarction. We therefore evaluated the response of plasma catecholamines to propranolol in 35 patients with acute myocardial infarction and compared the results with those obtained after placebo drug.…”

Section: Introductionmentioning

confidence: 99%

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Mueller¹,

Ayres²

1980

J. Clin. Invest.

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Section: Introductionmentioning

confidence: 99%

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Mueller¹,

Ayres²

1980

J. Clin. Invest.

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“…It has been assumed in most of these investigations that the circulating concentrations of catecholamines are the same in both the control and the adrenoceptor blockade experiments. Recent studies have cast doubt on the accuracy of this assumption (Irving et al, 1974).…”

Section: Discussionmentioning

confidence: 99%

Effects of Adrenoceptor Blockade on Plasma Catecholamine Levels During Adrenaline Infusion

Britton

Irving

Wood³

1977

British J Pharmacology

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The present experiments investigate the effects of phenoxybenzamine and propranolol, singly and in combination, on plasma catecholamine levels in sheep receiving a three‐hour adrenaline infusion. Five groups of five anaesthetized sheep were studied for a period of 3 h each. One group acted as a control and received only a saline (0.9% w/v NaCl solution) infusion. A second group received a constant infusion of adrenaline (2 μg kg body weight−1 min−1). A third group received a similar adrenaline infusion, having been premedicated with phenoxybenzamine (1 mg/kg body weight). A fourth group received a similar adrenaline infusion following premedication with (±)‐propranolol hydrochloride (7 μg/kg body weight). The fifth group received the adrenaline infusion following premedication with both the α‐ and β‐blocker in the above doses. Plasma catecholamines were measured on blood samples taken at seven intervals before, during and following the infusion. Control animals receiving only a saline infusion remained physiologically and biochemically stable throughout the experimental period. Adrenaline infusion in animals not receiving adrenoceptor blocking drugs caused a rise in plasma adrenaline levels from a low basal value of 1 μg/litre to a maximum level of 19.8 μg/litre. Animals premedicated with phenoxybenzamine exhibited a similar response. Animals premedicated with propranolol before the infusion of adrenaline did not demonstrate as marked a rise of plasma adrenaline levels as the two previous groups. The maximum mean plasma adrenaline level recorded in this group was 6.88 μg/litre. Animals premedicated with phenoxybenzamine and propranolol before the infusion of adrenaline showed only a small rise in plasma adrenaline levels compared with animals receiving adrenaline infusion alone. The maximum mean plasma adrenaline level in the group was only 3.43 μg/litre. The studies demonstrate that by an unknown mechanism β‐adrenoceptor blockade with (±)‐propranolol, either alone or in combination with phenoxybenzamine, lowers the plasma adrenaline response evoked by adrenaline infusion.

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“…Both ,B-selective and non-selective 3-adrenoceptor antagonists augment adrenaline levels during exercise (Gullestad et al, 1989b;Irving et al, 1971), and this may stimulate 132-adrenoceptors in the myocardium directly at maximal exercise. Accordingly, the reduction in peak heart rate response by non-selective ,B-adrenoceptor blockers may be due to blockade of the 12-as well as 13l-adrenoceptors (Friedman et al, 1987).…”

Section: Heart Ratementioning

confidence: 99%

Effects of selective beta 2‐adrenoceptor blockade on serum potassium and exercise performance in normal men.

Gullestad

Birkeland

Nordby

et al. 1991

Brit J Clinical Pharma

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3 Cumulative work was significantly reduced by ICI-118551 (6.4%, P = 0.04) and by propranolol (12.4%, P < 0.01), whereas the reduction with atenolol (5.6%) did not reach statistical significance. 4 Atenolol and propranolol reduced peak heart rate by 23% and 29%, and peak systolic blood pressure by 9% and 11% respectively during maximal exercise. ICI-118551 caused a non-significant reduction in heart rate during submaximal exercise, with a significant reduction at maximum exercise (6% reduction), whereas systolic blood pressure was not different from placebo. Diastolic blood pressures were similar across all treatment regimens. 5 Similar glucose concentrations were obtained at baseline and at exhaustion during all treatment regimens. Lactate concentrations were comparable for any given exercise intensity irrespective of treatment regimens. Propranolol reduced lactate concentrations from the exercising muscles at maximum exercise in proportion to the reduction of maximal exercise capacity.6 The subjective perception of fatigue was not affected by either 13l-or P2-adrenoceptor blockade.7 In a separate study, the effects of selective P2-adrenoceptor stimulation (terbutaline) in resting men on heart rate, systolic blood pressure, serum potassium and glucose were completely blocked by the doses of ICI-118551 used in the exercise study.8 We conclude that both ,l-and ,32-adrenoceptors are of importance for maximal short term exercise performance in healthy young men. The decisive mechanism for the reduction in exercise performance during ,-adrenoceptor blockade is unclear.The present study suggests that other mechanisms than haemodynamic and metabolic factors are of importance. The lack of effect of selective ,32-adrenoceptor antagonists on serum potassium at rest and during exercise, and the finding that the rate of decline in the potassium concentrations after exhaustion was independent of treatment regimens, suggests that ,3-adrenoceptors are of minor importance for potassium release or reuptake in the exercising muscle.

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Effects of β adrenergic blockade on plasma catecholamines in exercise

Cited by 103 publications

References 8 publications

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Effects of Adrenoceptor Blockade on Plasma Catecholamine Levels During Adrenaline Infusion

Effects of selective beta 2‐adrenoceptor blockade on serum potassium and exercise performance in normal men.

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