Findings from this investigation, demonstrate that, in acute stretch, Ca2+-mediating function of TRPC-6 was consequentially enhanced via [Ca2+]i, and endocardial TRPC-6 regulatory feedback protects against this stretch-induced myocardial Ca2+ overload process, whereas in chronic stretch, reduced protein expression of endocardial TRPC-6 and irregular Ca2+ transient cyclic events may lead to enhanced susceptibility to arrhythmia. The gene discussed is TRPC6; the disease is Arrhythmia.