The function of the aortic root is dependent upon its dynamic properties and interactions between its different structures. In an attempt to define which structures have the ability to alter their size and shape in response to humoral agents we examined the contractile capacity of the aortic root. In this respect endothelin has been shown to be present in the valve cusps and to mediate contraction of the cusp tissue by ETA and ETB receptors (Misfeld et al 2002). We wish to examine if aortic root structures possess contractile properties and if endothelin has the capacity to modulate the movements of the other components of the aortic root. Methods: Porcine aortic roots were removed and sectioned in a cryostat, and stained using an antibody to localise Immunohistochemical examination of each structure with an antibody raised against a-smooth muscle cell actin revealed the presence of positively stained fibres throughout sections of annular, sinus and sinotubular junction. Addition of KCl to isolated valve structures gave a mean contractile response of 0.63±0.07mN for cusp (n=7) mean ±SEM, 1.25±0.07mN for annular (n=15), 6.07±1.92mN for sinus (n=6) and 6.75±1.32mN for sinotubular junction (n=15). In a similar manner ET-1 induced concentration-dependent contraction in all structures. The magnitude of these responses was 0.87 ±0.14mN in the annulus, 0.90 ±0.14mN in the cusp, 2.15 ±0.68mN in the sinotubular junction to 3.95 ±1.28mN in the sinus wall. The potency (pEC50) of ET-1 was 5.60 for the cusp, 6.00 for the annulus, 6.70 for the sinus and 6.90 for the sinotubular junction. When normalised to potassium chloride the response to endothelin was significantly greater in the cusp compared to all other structures. These results demonstrate that all the structures that comprise the aortic root possess contractile properties. Endothelin is capable of inducing contraction throughout the aortic root and may therefore possess the capacity to regulate the coordinated movements of the aortic root structures during the cardiac cycle. Misfeld M, et al. J Heart Valve Dis. 2002 Jul;11(4):472-6; discussion 476-7. |