Review: Arterial stiffness and the renin-angiotensin-aldosterone system

Abstract

Arterial stiffness has recently been recognised as an independent risk factor for cardiovascular morbidity and mortality in hypertension. Many of the complications seen with angiotensin II (Ang II) excess or hyperaldosteronism -an increased event rate, left ventricular hypertrophy, endothelial dysfunction and target organ damage -are also associated with arterial stiffness. It is possible that reduced arterial compliance may be one mechanism whereby increased activity of the renin-angiotensin-aldosterone system (RAAS) produces adverse vascular effects. Common pathophysiological processes, altered collagen turnover and increased fibrosis may underlie both arterial stiffness and RAAS-associated vascular damage.While it is recognised that patients with hyperaldosteronism have increased arterial stiffness, the role of the RAAS in modulating arterial compliance in essential hypertension and in normotensive subjects is less clear cut. There is, however, more consistent data which show that drugs that interfere with Ang II or aldosterone, namely angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and aldosterone antagonists, all reduce arterial stiffness. In many cases, this is to a greater extent than predicted from the extent of reduction in blood pressure (BP), suggesting a role for RAAS in vascular stiffness in hypertensive subjects. There is also evidence that combined ACE inhibitors (ACE-Is) and ARBs may have an additive effect in reducing stiffness. The reduction in cardiovascular mortality in end-stage renal disease patients treated with ACE-Is was preferentially seen in those who had reduced arterial stiffness. These data suggest that, in addition to regulation of vascular biology and BP, the RAAS is an important determinant of arterial stiffness in health and, more particularly, in disease. IntroductionThe pulse has retained a central role throughout the history of medicine. It was, however, more an art than a science until the 19th century, when sphygmography provided the first graphic recordings of the arterial pressure pulse. Abnormalities in the pulse wave contour were considered indicative of stiff arteries and subsequently used to diagnose hypertension and Bright's disease.About the same time as Tigerstedt and Bergman discovered renin, sphygmography was abandoned in favour of cuff sphygmomanometry. There has been a recent awakening in the field of arterial stiffness follow-

Association of ambulatory arterial stiffness index with sEPCR in newly diagnosed hypertensive patients

“…In addition, activation of the RAS is associated with endothelial dysfunction and arterial stiffness. 34,35 Our finding that the levels of sEPCR and AASI were increased in the hypertensive patients versus healthy controls is consistent with this report. In the light of these studies, RAS activation might be one of the mechanisms that is responsible for increased sEPCR and arterial stiffness.…”

Angiotensin-Converting Enzyme Inhibitor or Angiotensin II Type 1 Receptor Antagonist Therapy Is Associated with Prolonged Patient and Graft Survival after Renal Transplantation

“…It may be hypothesized that similar to other clinical conditions that are associated with activation of the renin-angiotensin system and high vascular risk, the improvement of endothelial dysfunction by increased nitric oxide bioavailability and amelioration of neurohumoral activation may contribute partly to the observed effect (20). Furthermore, this class of agents exhibits beneficial effects on arterial stiffness independent of their antihypertensive potency (21). These may be explanations for why patients with ACEI/ARB therapy exhibited a reduced risk for CV death in our study.…”

Incremental value of arterial wave reflections in the determination of left ventricular diastolic dysfunction in untreated patients with essential hypertension

“…Thus, both small and large arteries contribute to early reflected waves. 3 In addition to advancing age, the combined effects of metabolic factors 41 endothelial dysfunction, 42 enhanced activity of the renin-angiotensin system, 43 increased circulating endothelin levels, low grade inflammation, 14,44 insulin resistance, 45 sodium retention induced by obesity, 36 atherosclerotic changes within the peripheral and coronary vessel wall 46 may all contribute to arterial stiffening and thus to the early arrival and increased amplitude of wave reflections as well as to LV diastolic dysfunction 3,14,16,36 in hypertensive individuals. Thus, increased arterial stiffness may represent an index of the cumulative effects of several other metabolic, neurohumoral, inflammatory factors, apart of aging, on the pathophysiological processes within the vascular and myocardial wall linking increased arterial stiffness and LV diastolic dysfunction.…”