Abstract
Suppressed nighttime blood pressure dipping is associated with salt sensitivity and may increase the hemodynamic load on the microvasculature. The mechanism remains unknown whereby salt sensitivity may increase the cardiovascular risk of non-dippers. Marinobufagenin, a novel steroidal biomarker, is associated with salt sensitivity and other cardiovascular risk factors independent of blood pressure. The authors investigated whether microvascular function in non-dippers is associated with marinobufagenin. The authors included 220 dippers and 154 non-dippers (aged 20-30 years) from the African-PREDICT study, with complete 24-hour urinary marinobufagenin and sodium data. The authors determined dipping status using 24-hour blood pressure monitoring and defined nighttime non-dipping <10%. The authors measured microvascular reactivity as retinal artery dilation in response to light flicker provocation. Young healthy non-dippers and dippers presented with similar peak retinal artery dilation, urinary sodium, and MBG excretion (P > .05). However, only in non-dippers did peak retinal artery dilation relate negatively to marinobufagenin excretion after single (r = -0.20; P = .012), partial (r = -0.23; P = .004), and multivariate-adjusted regression analyses (Adj. R2 = 0.34; β = -0.26; P < .001). The authors also noted a relationship between peak artery dilation and estimated salt intake (Adj. R2 = 0.30; β = -0.14; P = .051), but it was lost upon inclusion of marinobufagenin (Adj. R2 = 0.33; β = -0.015; P = .86). No relationship between microvascular reactivity and marinobufagenin was evident in dippers (P = .77). Marinobufagenin, representing salt sensitivity, may be involved in early microvascular functional changes in young non-dippers and thus contributes to the development of hypertension and cardiovascular disease later in life.