Physiological fluctuations of human plasma total salusin-β, an endogenous parasympathomimetic/proatherosclerotic peptide.

Salusin-β is an endogenous bioactive peptide that systemically exerts acute parasympathomimetic hemodynamic actions and locally induces atherogenesis. Due to its unique physicochemical characteristics to immediately adhere to all types of plastic and glassware, its plasma concentrations have only been successfully determined very recently. Using a total of 50 healthy adults (median age 28 years, range 24-57 years), we evaluated whether circulating salusin-β levels are affected by the autonomic nervous functions. Plasma total salusin-β levels obtained during daytime ambulatory monitoring of heart rate variability showed strong negative correlations with variables reflecting parasympathetic nervous activity, high frequency amplitude (HF; r=-0.27, p=0.0018) and the square root of the mean squared differences of successive normal-to-normal intervals (RMSSD; r=-0.19, p=0.0292), but did not with low frequency amplitude (LF) or LF/HF, variables influenced by sympathetic nervous activity. Because early morning nadir in the diurnal variation of plasma total salusin-β levels appeared to follow the nighttime parasympathetic nervous activity peak as quantified by HF and RMSSD, we determined whether parasympathetic stimulation reduces plasma salusin-β levels. Both Valsalva maneuver (p<0.05) and urination (p<0.05) significantly reduced plasma total salusin-β levels. Despite the fact that salusin-β is the sole endogenous parasympathomimetic peptide identified to date, the current results argue against the contention that physiological parasympathetic augmentation is the consequences of upregulated circulating salusin-β. Rather, circulating salusin-β levels are suppressed following physiological parasympathetic stimulation and appear to constitute a negative feedback relationship with the parasympathetic nervous system.