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Objective: We examined the arterial phenotype of semicarbazide-sensitive amine-oxidase null mouse (SSAO −/−) using various techniques including high resolution echotracking. Methods and results: SSAO −/− mice showed no change in arterial pressure under anesthesia. The in vivo arterial diameter, only measured in the carotid artery (CA), was higher in SSAO −/− than in SSAO +/+ animals. Elastic modulus–wall stress curves and CA rupture pressure were similar between SSAO −/− and +/+ mice, indicating no change in arterial wall stiffness or mechanical strength. There was no significant difference in insoluble elastin, total collagen content and elastic lamellar morphology between the two genotypes. No alteration in vascular reactivity was observed in aortic rings and mesenteric arteries from SSAO −/− mice. Aortic lysyl oxidase (LO) activity remained unaltered, indicating that SSAO invalidation is not accompanied by a compensatory increase in LO activity. Conclusion: This is the first functional study of arteries lacking SSAO. Our results indicate that SSAO −/− mice present an increased arterial diameter associated with normal arterial mechanical properties, suggesting that SSAO deficiency might contribute to arterial wall remodeling. However, these results argue against the hypothesis that SSAO intervenes in elastic fibre organization, elastin cross-linking processes and vasoreactivity.

Arterial stiffness is a cardiovascular risk factor that is independent of arterial pressure. Clinically, carotid-femoral pulse wave velocity (PWV) is the gold-standard parameter of arterial stiffness. Recent genetic studies have revealed specific genes that contribute to arterial stiffening. Here we review the recent findings on genome-wide linkage analyses and candidate gene polymorphism association studies. We also focus on the latest advances in the identification of gene variants affecting PWV using high density array single nucleotide polymorphism technology in a recent genome-wide association (GWA) study. Linkage and polymorphism studies revealed a first group of genes affecting the renin-angiotensin-aldosterone system, elastic fibre structural components, metalloproteinases, and the NO pathway. A second group of genes, identified by polymorphism association studies and possibly involved in the pathophysiology of arterial stiffness, includes beta-adrenergic receptors, endothelin receptors, and inflammatory molecules. The last group of genes, identified by GWA studies and unrelated to currently suspected mechanisms of arterial stiffness, may target transcriptional pathways controlling gene expression, differentiation of vascular smooth muscle cells, apoptosis of endothelial cells, or the immune response within the vascular wall.