The contribution of inflammation to the development of hypertension mediated by increased arterial stiffness

Background-the mechanisms underlying the possible contribution of chronic inflammation to the development of hypertension remain unclear. we examined the longitudinal association of inflammation with the progression of vascular and/or renal abnormalities in the development of hypertension. methods and results-in 3274 middle-aged japanese men without hypertension at the study baseline,brachial-ankle pulse wave velocity,blood pressure,estimated glomerular filtration rate,and serum crp (c reactive protein) levels were measured annually during a 9-year period. during this study period,474 participants (14.5%) developed hypertension. analysis of the repeatedmeasures data revealed that sustained elevation of serum crp levels was associated with a longitudinal increase of the brachialankle pulse wave velocity. a linear mixed model analysis revealed that higher log-transformed serum crp values (log crp) at each measurement were associated with a higher annual increase of the brachial-ankle pulse wave velocity (estimate= 32.553±11.635 cm/s per log crp,p=0.018),and that higher values of the brachial-ankle pulse wave velocity at each measurement were associated with a higher annual elevation of blood pressure (estimate=0.025±0.002 mm hg per log crp,p < 0.001). conclusions-in middle-aged japanese men without hypertension at study baseline,long-term active inflammation appears to be associated with a longitudinal increase of arterial stiffness. in turn,this longitudinal increase of arterial stiffness appears to be associated with longitudinal elevation of blood pressure to the hypertensive range. thus,systemic inflammation may play a role in the pathogenesis of hypertension by the progression of arterial stiffness. © 2017 the authors.