Material properties of the vessel wall in elastin mutant mice

The central feature that facilitates vessel elasticity is the apposition of smooth muscle cells and sheets (lamellae) of elastin in the arterial wall. To study how insufficiency of elastin alters vessel function, we generated mice hemizygous for the elastin gene (ELN+/−). Characterization of the arterial wall of these mice found that elastin haploinsufficiency results in changes in arterial wall structure, including thinner elastic lamellae and an increased number of smooth muscle cell layers. The animals are stably hypertensive with only mild cardiac hypertrophy and do not exhibit the hypertension‐induced arterial wall hypertrophy and decreased distensibility of large elastic arteries associated with essential hypertension. Studies of vessel mechanics and physiology show that the high blood pressure in elastin insufficiency is a developmental adaptation important for maintaining vessel patency appropriate to accommodate cardiac output and perfusion. These findings show that vascular smooth muscle cells are capable of altering vessel wall structure by sensing and responding to wall stress and that mechanical forces play an important role in determining lamellar number.