Large arteries in vertebrates serve as elastic reservoirs that store a portion of the blood volume with systole and discharge it during diastole. This function is made possible by the combination of extracellular matrix (ECM) proteins deposited by the smooth muscle cells (SMCs) in the arterial wall. Elastin and collagen expression in mice is first detectable around embryonic day 14 and peaks around postnatal day (P) 14, returning to baseline levels by P30. During this time, pressure and cardiac output increase significantly before leveling off ∼P30 [1]. Hence, the protein amounts and consequent mechanical properties of the arterial wall change simultaneously with the applied hemodynamic loads in a complicated and unknown feedback loop.

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