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Arterial stiffness (AS), as assessed via pulse wave velocity (PWV), is a major biomarker for cardiovascular risk assessment in patients with chronic kidney disease (CKD). However, the mechanisms responsible for the changes in PWV in the presence of kidney disease are not yet fully elucidated. In the present study, we aimed to investigate the direct effects attributable to biomechanical changes in the arterial tree caused by staged renal removal, independent of any biochemical or compensatory effects. Particularly, we simulated arterial pressure and flow using a previously validated one-dimensional (1-D) model of the cardiovascular system with different kidney configurations: two kidneys (2KDN), one single kidney (1KDN), no kidneys (0KDN), and a transplanted kidney (TX) attached to the external iliac artery. We evaluated the respective variations in blood pressure (BP), as well as AS of large-, medium-, and small-sized arteries via carotid-femoral PWV (cfPWV), carotid-radial PWV (crPWV), and radial-digital PWV (rdPWV), respectively. Our results showed that BP was increased in 1KDN and 0KDN, and that systolic BP values were restored in the TX configuration. Furthermore, a rise was reported in all PWVs for all tested configurations. The relative difference in stiffness from 2KDN to 0KDN was higher in the case of crPWV (15%) in comparison with the increase observed for cfPWV (11%). In TX, we observed a restoration of the PWVs to values close to 1KDN. Globally, it was demonstrated that alterations of the outflow boundaries to the renal arteries with staged kidney removal led to changes in BP and central and peripheral PWV in line with previously reported clinical data. Our findings suggest that the PWV variations observed in clinical practice with different stages of kidney disease may be partially attributed to biomechanical alterations of the arterial tree and their effect on BP.

Background: Physiologically, the aorta is less stiff than peripheral conductive arteries, creating an arterial stiffness gradient, protecting microcirculation from high pulsatile pressure. However, the pharmacological manipulation of arterial stiffness gradient has not been thoroughly investigated. We hypothesized that acute administration of nitroglycerin (NTG) may alter the arterial stiffness gradient through a more significant effect on the regional stiffness of medium-sized muscular arteries, as measured by pulse wave velocity (PWV). The aim of this study was to examine the differential impact of NTG on regional stiffness, and arterial stiffness gradient as measured by the aortic-brachial PWV ratio (AB-PWV ratio) and aortic-femoral PWV ratio (AF-PWV ratio).Methods: In 93 subjects (age: 61 years, men: 67%, chronic kidney disease [CKD]: 41%), aortic, brachial, and femoral stiffnesses were determined by cf-PWV, carotid-radial (cr-PWV), and femoral-dorsalis pedis artery (fp-PWV) PWVs, respectively. The measurements were repeated 5 min after the sublingual administration of NTG (0.4 mg). The AB-PWV and AF-PWV ratios were obtained by dividing cf-PWV by cr-PWV or fp-PWV, respectively. The central pulse wave profile was determined by radial artery tonometry through the generalized transfer function.Results: At baseline, cf-PWV, cr-PWV, and fp-PWV were 12.12 ± 3.36, 9.51 ± 1.81, and 9.71 ± 1.89 m/s, respectively. After the administration of NTG, there was a significant reduction in cr-PWV of 0.86 ± 1.27 m/s (p < 0.001) and fp-PWV of 1.12 ± 1.74 m/s (p < 0.001), without any significant changes in cf-PWV (p = 0.928), leading to a significant increase in the AB-PWV ratio (1.30 ± 0.39 vs. 1.42 ± 0.46; p = 0.001) and AF-PWV ratio (1.38 ± 0.47 vs. 1.56 ± 0.53; p = 0.001). There was a significant correlation between changes in the AF-PWV ratio and changes in the timing of wave reflection (r = 0.289; p = 0.042) and the amplitude of the heart rate-adjusted augmented pressure (r = − 0.467; p < 0.001).Conclusion: This study shows that acute administration of NTG reduces PWV of muscular arteries (brachial and femoral) without modifying aortic PWV. This results in an unfavorable profile of AB-PWV and AF-PWV ratios, which could lead to higher pulse pressure transmission into the microcirculation.