Myocardial adaptation to stress from the viewpoint of evolution and development.
Myocardial hypertrophy, which results from the increase in demand placed on the heart, does not involve the simple enlargement of the myocardial cell. Instead, the cells are restructured in a manner that depends on the nature of the stress applied. The cellular reorganization involves the contractile, EC coupling, and recovery systems. In the remodeling of each of these systems, a repertoire of functional adaptation is used which bears a remarkable similarity to the changes seen in the differentiation of species and the development of muscle type. Thus, in pressure overload hypertrophy, where the maintenance of persistent high pressure in a necessity, the contractile system of the muscle is slower and more economical. This is similar to the specialization seen in the tortoise or in slow muscles like the rat soleus. In thyrotoxic hypertrophy, where the demand is to move the blood at high velocity, the muscle is fast and less economical. This is similar to the specialization seen in the frog sartorius or rat EDL. The restructuring involves specific molecular changes that uniquely adapt the muscles for the tasks at hand.
D000222:Adaptation, Physiological; D000818:Animals; D001833:Body Temperature Regulation; D002118:Calcium; D006332:Cardiomegaly / Q000503:physiopathology*; D003285:Contractile Proteins / Q000378:metabolism; D009200:Myocardial Contraction; D011312:Pressure; D011817:Rabbits
D003285:Contractile Proteins; D002118:Calcium