TERTATOLOL POTENTIATES EXERCISE-INDUCED ATRIAL-NATRIURETIC-PEPTIDE RELEASE BY INCREASING ATRIAL DIAMETER IN HEALTHY-SUBJECTS

To evaluate the contribution of atrial distension and/or adrenergic me chanisms in the regulation of atrial natriuretic peptide (ANP) secreti on, plasma immunoreactive ANP, norepinephrine (NE), epinephrine (E), a nd left atrial diameter were measured at rest, during, and after grade d upright standardised bicycle exercise in 8 healthy male subjects aft er single-dose administration of placebo, tertatolol (5 mg), prazosin (1 mg), or combination of tertatolol (5 mg) and prazosin (1 mg). Systo lic and diastolic left atrial diameters were measured before, during, and just after exercise by bidimensional echocardiography. Exercise ra ised plasma ANP concentrations. This rise was greater on tertatolol al one and tertatolol and prazosin than on placebo or prazosin alone: mea n area under the plasma ANP concentration curve increased by 35% on te rtatolol alone, 45% on tertatolol and prazosin when compared with plac ebo (p < 0.01), and by 82 and 94%, respectively, when compared with pr azosin alone (p < 0.01). The rise in plasma ANP was greater during the postexercise period: 80% for tertatolol alone, 67% for tertatolol and prazosin when compared with placebo (p < 0.01) and 133 and 115%, resp ectively, when compared with prazosin alone (p < 0.01). The rise in pl asma ANP was accompanied by an increase in both systolic and diastolic atrial diameters which was significantly greater on tertatolol alone and on the tertatolol and prazosin combination than on placebo or praz osin alone (p < 0.001). Beta-blockade alone did not affect plasma cate cholamine concentrations but exercise-induced increase in plasma NE wa s significantly potentiated by prazosin and the prazosin and tertatolo l combination, and that of plasma E by the prazosin and tertatolol com bination. We conclude that potentiation of exercise-induced plasma ANP increase by tertatolol may be due to atrial stretch consequent upon t he decreased myocardial contractility and relaxation and not to alpha1 -adrenoceptor stimulation, and that increase in plasma catecholamines does not play an important role in ANP secretion.