Vertebrate hearts are broadly classified by the presence or absence of coronary circulation, and highly active and energy-consuming animals have coronary circulation. Blood flow occurs mostly during diastole in coronary circulation because vascular compression limits flow during systole. Therefore, the hearts with coronary circulation should have stiffer mechanical property to prevent excessive extensions of the heart during diastole resulting in a reduction of blood flow. To understand the molecular mechanism of extension restriction of coronary circulation hearts, we focused on connectin/titin, which regulates the extensibility of cardiac cells by generating passive tension during diastole. We found the lengths of PEVK and N2B regions of connectin, which function as molecular springs, were enormously shorter in the hearts with coronary circulation (mammalians and birds) than that with sinusoidal circulation (amphibians). These results indicate that the shorter elastic regions of connectin may contribute to the extension restriction of hearts with coronary circulation.
