ISSN:
1432-1041
Keywords:
β-Adrenoceptor-blockade
;
α1-Adrenoceptor blockade
;
Atrial natriuretic peptide
;
exercise
;
atrial distension
;
plasma catecholamines
;
prazosin
;
tertatolol
Source:
Springer Online Journal Archives 1860-2000
Topics:
Chemistry and Pharmacology
,
Medicine
Notes:
Summary The role of atrial distension and/or adrenergic mechanisms in the regulation of atrial natriuretic peptide (ANP) secretion, plasma immunoreactive ANP, norepinephrine (NE), epinephrine (E) and left atrial diameter at rest, during and after graded bicycle exercise has been studies in 8 healthy male subjects after single doses of placebo, tertatolol 5 mg (a non-selective β-adrenoceptor blocker), prazosin 1 mg (an α1-adrenoceptor antagonist) and their combination. Systolic and diastolic left atrial diameters were measured before, during and just after exercise by bidimensional echocardiography. Exercise caused an increase in plasma ANP, which was greater after tertatolol alone, and tertatolol plus prazosin, than after placebo or prazosin alone; the mean area under the plasma ANP concentration curve was increased by 35% after tertatolol alone, by 45% after tertatolol and prazosin compared to placebo, and by 82% and 94%, respectively when compared to prazosin alone. The rise in plasma ANP was more marked during the post-exercise period: 80% after tertatolol alone, 67% after tertatolol and prazosin compared to placebo, and 133% and 115%, respectively, compared to prazosin alone. The rise in plasma ANP was accompanied by an increase in both the systolic and diastolic atrial diameter, which was also significantly greater after tertatolol alone and the combination than placebo, or after prazosin alone. β-Adrenoceptor blockade alone did not affect the plasma catecholamine concentrations, but the exercise-induced increase in plasma norepinephrine was significantly potentiated by prazosin and by prazosin plus tertatolol, and that of plasma epinephrine by the drug combination. We conclude that potentiation of the exercise-induced increase in plasma ANP by β-blockers may be due to atrial stretching consequent on the decreased myocardial contractility and relaxation, and not to alpha-1 adrenoceptor stimulation. Any increase in plasma catecholamines did not play an important role in ANP secretion.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00315469
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