C-type natriuretic peptide plasma levels and whole blood mrna expression show different trends in adolescents with different degree of endothelial dysfunction

C-type natriuretic peptide (CNP) is an endogenous adipogenesis regulator whose plasma levels in childhood areknown, while no data are available on its expression. Our aim was to evaluate both CNP plasma levels and CNPsystem expression in whole blood obtained from normal-weight (N, n = 24) and obese (O, n = 16) adolescents(age:13.5 ± 0.4 years). Endothelial function was assessed measuring reactive hyperemia index (RHI). CNPplasma levels, evaluated with specific RIA, resulted significantly lower in O than in N (6.1 ± 0.8 vs.15.2 ±1.3 pg/mL; p < 0.0001), while CNP/NPR-B/NPR-C mRNA, measured by Real-Time PCR, resulted similar in N(4.1 ± 1.7; 5.0 ± 1.6; 2.2 ± 0.9) and in O (4.3 ± 1.6; 3.5 ± 1.1; 2.3 ± 0.8). RHI was significantly lower inO than in N (1.4 ± 0.08 vs.2.1 ± 0.04, p < 0.0001). Dividing all subjects according to the RHI median value,irrespective of the presence or absence of obesity (Group 1 > 1.9, n = 23, Group 2 < 1.9, n = 17), CNP plasmaconcentrations resulted significantly (p = 0.014) higher in Group 1 (14.6 ± 1.6) than in Group 2 (7.5 ± 1.0),showing a significant correlation with RHI (p = 0.0026), while CNP mRNA expression was, surprisingly, higherin Group 2 (7.0 ± 2.3) than in Group 1 (1.8 ± 0.4; p = 0.02). NPR-B mRNA resulted similar in both Groups(4.3 ± 1.6; 4.7 ± 1.3) and NPR-C significantly higher in Group 2 (p = 0.02). Our data suggest different trendsbetween CNP plasma levels and expression, assessed for the first time in whole blood, that could reflect changesoccurring both at CNP transcriptional level in activated leukocytes due to inflammation, and at circulatinglevels, due to CNP paracrine/autocrine activities. This could represent an interesting area for new therapies ableto modulate endothelial dysfunction.