Introduction Noninvasive measures of atherosclerosis have become established tools for cardiovascular risk prediction, largely studied in older individuals. Pulse pressure (PP) is a simple surrogate measure of arterial stiffness, while Ambulatory Arterial Stiffness Index (AASI) is a relatively new vascular compliance measure calculated as 1 minus the regression slope of DBP over SBP readings obtained from 24 hour ambulatory blood pressure monitoring (ABPM). We examined the hypothesis: PP and AASI correlate with blood pressure (BP), along with microvascular and endothelial function, in young adult normotensive and prehypertensive subjects. Methods 24 hour BP, PP, and AASI were calculated from ABPM, and clinic BP obtained in 140 subjects (87 female, 53 male; 117 non-black, 23 black) with mean +/- sd age 26 +/- 6 years. Strain gauge plethysmography was used to assess endothelial function. Microvascular function was measured with direct capillaroscopy visualization of capillaries. Pearson correlation coefficients and multiple linear regression were used to analyze BP, microvascular, and endothelial function as predictors of PP and AASI, controlling for BMI, gender, age and race. Results PP and AASI are correlated (r=0.59; p<0.001). Both PP and AASI were significantly associated with ABPM and clinic SBP measures (SBP24: p=0.001/p=0.002; SBP daytime: p=0.001/p=0.009; SBP clinic: p=0.001/p=0.047; p values =PP/AASI). No association was seen for any measures with DBP. Both PP (p=0.08) and AASI (p=0.056) were marginally associated with endothelial function, while only AASI was significantly associated with microvascular function (p=0.027) along with BP dipping (drop of 10% or more during sleep: SBP and DBP p<0.001), another known predictor of cardiovascular risk. Conclusions In conclusion, both PP and AASI are associated with SBP in young normotensive and prehypertensive patients, indicating potential usefulness of these measures for early identification of arterial stiffness and associated cardiovascular risk, prior to development of established hypertension. Microvascular and endothelial dysfunction may contribute to the pathophysiology underlying higher PP/AASI values, with AASI more closely correlated with these processes.