Relationship between urinary salt excretion and pulse pressure and central aortic hemodynamics independent of steady state pressure in the general population.

Although central pulse pressure (PPc) is strongly related to central mean arterial pressure (MAPc), PPc predicts cardiovascular outcomes beyond MAPc. Whether modifiable risk factors for hypertension contribute to PPc and its determinants, independent of MAPc, is uncertain. In 635 randomly recruited participants, we assessed the independent relationship between 24-hour urinary sodium (Na(+)) or potassium (K(+)) excretion and brachial artery PP (in office or 24-hour; n = 487), PPc, the forward (P1) and augmented (Paug) pressure wave components of PPc, central augmentation index, and determinants of central pressure waves, including aortic pulse wave velocity, effective reflecting distance, and reflective wave transit time. Central dynamics were determined using applanation tonometry of the carotid, femoral, and radial arteries. With adjustments for potential confounders, urinary Na(+)/K(+) was independently associated with in-office, central, and 24-hour PP, as well as Paug, P1, and central augmentation index (P<0.05 to P<0.005). With further adjustments for MAPc (or diastolic BP), urinary Na(+)/K(+) was independently associated with PPc, 24-hour PP, Paug, P1, and central augmentation index (P<0.05 to P = 0.005) but not with in-office PP, pulse wave velocity, effective reflecting distance, or reflective wave transit time. In conclusion, in a population of African ancestry, urinary salt excretion is independently related to central and 24-hour PP independent of MAPc or diastolic BP, effects that are attributed to increases in both P1 and Paug but not to pulse wave velocity. Hence, modifying salt intake could influence cardiovascular risk through effects on 24-hour and central PPs, as well as P1 and Paug, independent of steady-state pressure (MAP or diastolic BP) or pulse wave velocity.