BACKGROUND: Metabolic abnormalities in obesity can overstimulate the renal epithelial sodium channel (ENaC) and subsequently lead to blood pressure (BP) elevation. Prostasin, a membrane-bound/secretive serine protease, is thought to activate ENaC via the proteolytic cleavage of the channel. Our specific aim was to explore whether there is a relationship between adiposity and urinary prostasin excretion at the population level. METHODS: In 271 African-American adolescents, urinary prostasin concentrations were determined by enzyme-linked immunosorbent assay and normalized by urinary creatinine. RESULTS: Urinary prostasin excretion increased in the overweight/obese group (n = 110, 38.2 ± 4.0 ng/mg) vs. the normal-weight group (n = 161, 20.7 ± 1.2 ng/mg, P = 0.03). Urinary prostasin excretion was significantly correlated with BMI percentiles (r = 0.14, P = 0.02), waist circumference (r = 0.13, P = 0.05), total body fat mass (r = 0.20, P < 0.01), and percentage body fat (r = 0.23, P < 0.01). Urinary prostasin excretion was also correlated with plasma aldosterone (r = 0.11, P = 0.05) and systolic BP (SBP; r = 0.15, P = 0.02), but the significances disappeared after adjustment of any of the adiposity variables. CONCLUSION: Our data for the first time suggest that adiposity plays a role in urinary prostasin excretion, and its associations with aldosterone and BP appear to be modulated by adiposity. Whether urinary prostasin excretion is a biomarker/mechanism underlying obesity-related hypertension deserves further investigations.
BACKGROUND:Metabolic abnormalities in obesity can overstimulate the renal epithelial sodium channel (ENaC) and subsequently lead to blood pressure (BP) elevation. Prostasin, a membrane-bound/secretive serine protease, is thought to activate ENaC via the proteolytic cleavage of the channel. Our specific aim was to explore whether there is a relationship between adiposity and urinary prostasin excretion at the population level. METHODS: In 271 African-American adolescents, urinary prostasin concentrations were determined by enzyme-linked immunosorbent assay and normalized by urinary creatinine. RESULTS: Urinary prostasin excretion increased in the overweight/obese group (n = 110, 38.2 ± 4.0 ng/mg) vs. the normal-weight group (n = 161, 20.7 ± 1.2 ng/mg, P = 0.03). Urinary prostasin excretion was significantly correlated with BMI percentiles (r = 0.14, P = 0.02), waist circumference (r = 0.13, P = 0.05), total body fat mass (r = 0.20, P < 0.01), and percentage body fat (r = 0.23, P < 0.01). Urinary prostasin excretion was also correlated with plasma aldosterone (r = 0.11, P = 0.05) and systolic BP (SBP; r = 0.15, P = 0.02), but the significances disappeared after adjustment of any of the adiposity variables. CONCLUSION: Our data for the first time suggest that adiposity plays a role in urinary prostasin excretion, and its associations with aldosterone and BP appear to be modulated by adiposity. Whether urinary prostasin excretion is a biomarker/mechanism underlying obesity-related hypertension deserves further investigations.
Authors: R W Scott; B L Bergman; A Bajpai; R T Hersh; H Rodriguez; B N Jones; C Barreda; S Watts; J B Baker Journal: J Biol Chem Date: 1985-06-10 Impact factor: 5.157
Authors: Dexter L Lee; Lashon C Sturgis; Hicham Labazi; James B Osborne; Cassandra Fleming; Jennifer S Pollock; Marlina Manhiani; John D Imig; Michael W Brands Journal: Am J Physiol Heart Circ Physiol Date: 2005-11-11 Impact factor: 4.733