The present retrospective analysis of data derived from a population-based study examined
the relationship between intake of beta-receptor antagonists and plasma concentrations
of the cardiac natriuretic peptides and their second messenger.
Beta-receptor antagonists are widely used for treatment of cardiovascular disease.
In addition to direct effects on heart rate and cardiac contractility, recent evidence
suggests that beta-receptor antagonists may also modulate the cross talk between the
sympathetic nervous system and the cardiac natriuretic peptide system.
Plasma concentrations of atrial natriuretic peptide (ANP), brain natriuretic peptide
(BNP) and their second messenger cyclic guanosine monophosphate (cGMP) were assessed
in addition to anthropometric, hemodynamic and echocardiographic parameters in a population-based
sample (n = 672), of which 80 subjects used beta-receptor antagonists.
Compared to subjects without medication, subjects receiving beta-receptor antagonists
were characterized by substantially elevated ANP, BNP and cGMP plasma concentrations
(plus 32%, 89% and 18%, respectively, p < 0.01 each). Analysis of subgroups revealed
that this effect was highly consistent and present even in the absence of hypertension,
left atrial enlargement, left ventricular hypertrophy or left ventricular dysfunction.
The most prominent increase was observed in a subgroup with increased left ventricular
mass index. By multivariate analysis, a statistically significant and independent
association between beta-receptor antagonism and ANP, BNP and cGMP concentrations
was confirmed. Such an association could not be demonstrated for other antihypertensive
agents such as angiotensin-converting enzyme inhibitors or diuretics.
Beta-receptor antagonists appear to augment plasma ANP, BNP and cGMP concentrations.
The current observation suggests an important contribution of the cardiac natriuretic
peptide system to the therapeutic mechanism of beta-receptor antagonists.