Single cardiac cell studies highlight the role of stretch-activated channels in arrhythmias and the importance of angiotensin II in stretch-induced hypertrophy.
This brief review looks at recent work investigating length-dependent mechanisms in single cardiac cells. Studies using the mechanically simple single cardiac cell have confirmed much of the data previously reported in multicellular preparations, although some differences between single cell and multicellular studies have been found. Electrical studies have been able to investigate the effects of stretch on ion channels and have concentrated upon the exciting discovery of many types of stretch-activated channels in the heart. These channels may explain the occurrence of length-dependent changes in pacemaker activity and stretch-activated arrhythmias in the whole heart. Prolonged stretch can lead to hypertrophy, and single cell studies have been able to characterize the sequence of events leading from membrane stretch to altered protein expression. It appears from these studies that the role of angiotensin II is important.
Ed White (Fri,) conducted a review in Cardiac cell physiology. Stretch / length-dependent mechanisms was evaluated. Single cardiac cell studies highlight the role of stretch-activated channels in arrhythmias and the importance of angiotensin II in stretch-induced hypertrophy.