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Augmentation of the cardiac natriuretic peptides by beta-receptor antagonism: evidence from a population-based study

Andreas Luchner, MD^a, John C. Burnett, Jr., MD^*, Michihisa Jougasaki, MD, PhD^*, Hans-Werner Hense, MD , G.ünter A. J. Riegger, MD^a and Heribert Schunkert, MD^a

^a Klinik und Poliklinik für Innere Medizin II, University of Regensburg, Regensburg, Germany
^* Cardiorenal Research Laboratory, Mayo Clinic, Rochester, Minnesota, USA
GSF-Institut für Epidemiologie, Munich, Germany
Institut für Epidemiologie und Sozialmedizin, University of Münster, Münster, Germany

View larger version (18K): [in a new window]   Figure 1 Atrial natriuretic peptide, brain natriuretic peptide, and cyclic guanosine monophosphate plasma concentrations were significantly elevated in subjects with (black bars) as compared to those without (hatched bars) beta-receptor antagonism. Differences between groups may be overestimated by confounding variables (Table 2). ANP and BNP were in pg·ml–1 and cGMP in pmol·ml–1. **p < 0.01 vs. subjects without beta-receptor antagonism.

View larger version (45K): [in a new window]   Figure 2 Subgroup analysis for ANP and BNP plasma concentrations in subjects with (black bars) and without (hatched bars) beta-receptor antagonism. RR = arterial blood pressure; Rx = antihypertensive therapy; LAd = left atrial diameter; LVMI = left ventricular mass index; LV-fct. = left ventricular function. *p < 0.05 vs. subjects without beta-receptor antagonism, **p < 0.01 vs. subjects without beta-receptor antagonism.