Stress-Induced Sodium Excretion

Abstract

Impaired stress-induced pressure natriuresis, ie, an inadequate compensatory increase in urinary sodium excretion (U Na V) in response to a stress-induced blood pressure increase, may lead to the premature development of essential hypertension. To assess the heritability of baseline U Na V, stress U Na V, and the U Na V response to stress (ΔU Na V=stress U Na V− baseline U Na V), we studied 396 black and 494 white twins, including monozygotic and dizygotic twins of the same as well as the opposite sex (mean age: 17.6±3.3 years; range: 11.9 to 30.0 years). Bivariate genetic model fitting was performed to examine the extent to which genetic and environmental factors are common or specific to baseline and stress U Na V. Heritability estimates for ΔU Na V can be derived from these bivariate models. All of the bivariate analyses were performed separately in whites and blacks, because univariate models for baseline U Na V showed significant ethnic differences in heritability estimates. Best-fitting models showed that the heritability of stress U Na V was 0.42 in whites and 0.58 in blacks. Only 15% and 11% of the total variance could be attributed to genetic factors common to baseline and stress U Na V in whites and blacks, respectively. After removal of all of the shared influences with baseline U Na V, heritabilities for stress U Na V were 0.32 in whites and 0.57 in blacks. Heritability estimates for ΔU Na V were 0.36 in whites and 0.39 in blacks. In summary, this study establishes ΔU Na V and stress U Na V as heritable phenotypes that may be used to study the genetic etiology of early hypertension development.