Pulse pressure, arterial stiffness, and end-organ damage

Abstract

Whereas larger arteries participate in the dampening of blood pressure (BP) oscillations resulting from intermittent ventricular ejection, smaller arteries steadily deliver an adequate supply of blood from the heart to the peripheral organs. Numerous active mechanisms are involved in this process. Cyclic stress acts differently from steady stress, inducing stronger and stiffer material of the vessel wall than under static conditions. Cyclic strain participates in the phenotypic plasticity of smooth muscle cells, initiates transduction mechanisms and induces the transcriptional profile of mechanically induced genes. Finally, the autoregulatory mechanism protecting the brain, heart and kidney from cardiovascular (CV) damage differ markedly according to their localization. Whereas the heart is dependent on pulsatile forces, owing to the diastolic perfusion of coronary arteries, the brain and the kidney are rather influenced by steady mechanical forces. For the kidney, the transmission of pulsatile pressure may greatly contribute to glomerular sclerosis in the elderly.